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Medical Physiology E-Book

Medical Physiology E-Book

Walter F. Boron | Emile L. Boulpaep

(2016)

Additional Information

Book Details

Abstract

For a comprehensive understanding of human physiology — from molecules to systems —turn to the latest edition of Medical Physiology. This updated textbook is known for its unparalleled depth of information, equipping students with a solid foundation for a future in medicine and healthcare, and providing clinical and research professionals with a reliable go-to reference. Complex concepts are presented in a clear, concise, and logically organized format to further facilitate understanding and retention.

  • Clear, didactic illustrations visually present processes in a clear, concise manner that is easy to understand.
  • Intuitive organization and consistent writing style facilitates navigation and comprehension.
  • Takes a strong molecular and cellular approach that relates these concepts to human physiology and disease.
  • An increased number of clinical correlations provides a better understanding of the practical applications of physiology in medicine.
  • Highlights new breakthroughs in molecular and cellular processes, such as the role of epigenetics, necroptosis, and ion channels in physiologic processes, to give insights into human development, growth, and disease.
  • Several new authors offer fresh perspectives in many key sections of the text, and meticulous editing makes this multi-authored resource read with one unified voice.
  • Includes electronic access to 10 animations and copious companion notes prepared by the Editors.

Table of Contents

Section Title Page Action Price
Front Cover cover
Inside Front Cover ifc1
IFC_International edition IFC1
Medical Physiology i
Copyright Page iv
Contributors v
Video Table of Contents vi
Preface to the Third Edition vii
The eBook vii
Acknowledgments vii
Preface to the First Edition ix
Target Audience ix
Content of the Textbook ix
Emphasis of the Textbook ix
Creating the Textbook ix
Special Features x
Acknowledgments x
Table Of Contents xi
I Introduction 1
1 Foundations of Physiology 2
What is physiology? 2
Physiological genomics is the link between the organ and the gene 2
Cells live in a highly protected milieu intérieur 3
Homeostatic mechanisms—operating through sophisticated feedback control mechanisms— are responsible for maintaining the constancy of the milieu intérieur 4
Medicine is the study of “physiology gone awry” 4
References 5
References 5.e1
II Physiology of Cells and Molecules 7
2 Functional Organization of the Cell 8
Structure of Biological Membranes 8
The surface of the cell is defined by a membrane 8
The cell membrane is composed primarily of phospholipids 8
Phospholipids form complex structures in aqueous solution 9
The diffusion of individual lipids within a leaflet of a bilayer is determined by the chemical makeup of its constituents 10
Phospholipid bilayer membranes are impermeable to charged molecules 11
The plasma membrane is a bilayer 12
Membrane proteins can be integrally or peripherally associated with the plasma membrane 13
The membrane-spanning portions of transmembrane proteins are usually hydrophobic α helices 13
Some membrane proteins are mobile in the plane of the bilayer 15
Function of Membrane Proteins 16
Integral membrane proteins can serve as receptors 16
Integral membrane proteins can serve as adhesion molecules 17
Integral membrane proteins can carry out the transmembrane movement of water-soluble substances 17
Integral membrane proteins can also be enzymes 18
Integral membrane proteins can participate in intracellular signaling 18
Peripheral membrane proteins participate in intracellular signaling and can form a submembranous cytoskeleton 18
Cellular Organelles and the Cytoskeleton 20
The cell is composed of discrete organelles that subserve distinct functions 20
The nucleus stores, replicates, and reads the cell’s genetic information 21
Lysosomes digest material derived from the interior and exterior of the cell 22
The mitochondrion is the site of oxidative energy production 22
The cytoplasm is not amorphous but is organized by the cytoskeleton 22
Intermediate filaments provide cells with structural support 23
Microtubules provide structural support and provide the basis for several types of subcellular motility 23
Thin filaments (actin) and thick filaments (myosin) are present in almost every cell type 25
Synthesis and Recycling of Membrane Proteins 28
Secretory and membrane proteins are synthesized in association with the rough ER 28
Simultaneous protein synthesis and translocation through the rough ER membrane requires machinery for signal recognition and protein translocation 28
Proper insertion of membrane proteins requires start- and stop-transfer sequences 30
Newly synthesized secretory and membrane proteins undergo post-translational modification and folding in the lumen of the rough ER 32
Secretory and membrane proteins follow the secretory pathway through the cell 34
Carrier vesicles control the traffic between the organelles of the secretory pathway 35
Specialized protein complexes, such as clathrin and coatamers, mediate the formation and fusion of vesicles in the secretory pathway 35
Vesicle Formation in the Secretory Pathway 35
Vesicle Fusion in the Secretory Pathway 37
Newly synthesized secretory and membrane proteins are processed during their passage through the secretory pathway 37
Newly synthesized proteins are sorted in the trans-Golgi network 39
A mannose-6-phosphate recognition marker is required to target newly synthesized hydrolytic enzymes to lysosomes 40
Cells internalize extracellular material and plasma membrane through the process of endocytosis 40
Receptor-mediated endocytosis is responsible for internalizing specific proteins 42
Endocytosed proteins can be targeted to lysosomes or recycled to the cell surface 42
Certain molecules are internalized through an alternative process that involves caveolae 42
Specialized Cell Types 43
Epithelial cells form a barrier between the internal and external milieu 43
Tight Junctions 43
Adhering Junctions 44
Gap Junctions 45
Desmosomes 45
Epithelial cells are polarized 45
References 46
References 46.e1
Books and Reviews 46.e1
Journal Articles 46.e1
3 Signal Transduction 47
Mechanisms of Cellular Communication 47
Cells can communicate with one another via chemical signals 47
Soluble chemical signals interact with target cells via binding to surface or intracellular receptors 47
Cells can also communicate by direct interactions—juxtacrine signaling 50
Gap Junctions 50
Adhering and Tight Junctions 50
Membrane-Associated Ligands 50
Ligands in the Extracellular Matrix 50
Second-messenger systems amplify signals and integrate responses among cell types 50
Receptors That are Ion Channels 51
Ligand-gated ion channels transduce a chemical signal into an electrical signal 51
Receptors Coupled to G Proteins 51
General Properties of G Proteins 52
G proteins are heterotrimers that exist in many combinations of different α, β, and γ subunits 52
G-protein activation follows a cycle 53
Activated α subunits couple to a variety of downstream effectors, including enzymes and ion channels 53
βγ subunits can activate downstream effectors 56
Small GTP-binding proteins are involved in a vast number of cellular processes 56
G-Protein Second Messengers: Cyclic Nucleotides 56
cAMP usually exerts its effect by increasing the activity of protein kinase A 56
Protein phosphatases reverse the action of kinases 57
cGMP exerts its effect by stimulating a nonselective cation channel in the retina 58
G-Protein Second Messengers: Products of Phosphoinositide Breakdown 58
Many messengers bind to receptors that activate phosphoinositide breakdown 58
IP3 liberates Ca2+ from intracellular stores 60
Calcium activates calmodulin-dependent protein kinases 60
DAGs and Ca2+ activate protein kinase C 60
G-Protein Second Messengers: Arachidonic Acid Metabolites 61
Phospholipase A2 is the primary enzyme responsible for releasing AA 62
Cyclooxygenases, lipoxygenases, and epoxygenases mediate the formation of biologically active eicosanoids 62
Prostaglandins, prostacyclins, and thromboxanes (cyclooxygenase products) are vasoactive, regulate platelet action, and modulate ion transport N3-16 64
The leukotrienes (5-lipoxygenase products) play a major role in inflammatory responses 64
The HETEs and EETs (epoxygenase products) tend to enhance Ca2+ release from intracellular stores and to enhance cell proliferation 65
Degradation of the eicosanoids terminates their activity 65
Receptors That are Catalytic 66
The receptor guanylyl cyclase transduces the activity of atrial natriuretic peptide, whereas a soluble guanylyl cyclase transduces the activity of nitric oxide 66
Receptor (Membrane-Bound) Guanylyl Cyclase 66
Soluble Guanylyl Cyclase 66
Some catalytic receptors are serine/threonine kinases 67
RTKs produce phosphotyrosine motifs recognized by SH2 and phosphotyrosine-binding domains of downstream effectors 68
Creation of Phosphotyrosine Motifs 68
Recognition of pY Motifs by SH2 and Phosphotyrosine-Binding Domains 68
The MAPK Pathway 68
The Phosphatidylinositol-3-Kinase Pathway 69
Tyrosine kinase–associated receptors activate cytosolic tyrosine kinases such as Src and JAK 70
Receptor tyrosine phosphatases are required for lymphocyte activation 71
Nuclear Receptors 71
Steroid and thyroid hormones enter the cell and bind to members of the nuclear receptor superfamily in the cytoplasm or nucleus 71
Activated nuclear receptors bind to sequence elements in the regulatory region of responsive genes and either activate or repress DNA transcription 72
References 72
References 72.e1
Books and Reviews 72.e1
Journal Articles 72.e1
4 Regulation of Gene Expression 73
From Genes to Proteins 73
Gene expression differs among tissues and—in any tissue—may vary in response to external stimuli 73
Genetic information flows from DNA to proteins 73
The gene consists of a transcription unit 74
DNA is packaged into chromatin 75
Gene expression may be regulated at multiple steps 76
Transcription factors are proteins that regulate gene transcription 78
The Promoter and Regulatory Elements 78
The basal transcriptional machinery mediates gene transcription 78
The promoter determines the initiation site and direction of transcription 78
Positive and negative regulatory elements modulate gene transcription 79
Locus control regions and insulator elements influence transcription within multigene chromosomal domains 80
Transcription Factors 81
DNA-binding transcription factors recognize specific DNA sequences 81
Transcription factors that bind to DNA can be grouped into families based on tertiary structure 82
Zinc Finger 82
Basic Zipper 83
Basic Helix-Loop-Helix 83
Helix-Turn-Helix 83
Coactivators and corepressors are transcription factors that do not bind to DNA 83
Transcriptional activators stimulate transcription by three mechanisms 84
Recruitment of the Basal Transcriptional Machinery 84
Chromatin Remodeling 84
Stimulation of Pol II 85
Transcriptional activators act in combination 85
Transcriptional repressors act by competition, quenching, or active repression 85
The activity of transcription factors may be regulated by post-translational modifications 86
Phosphorylation 86
Site-Specific Proteolysis 87
Other Post-Translational Modifications 88
The expression of some transcription factors is tissue specific 88
Regulation of Inducible Gene Expression by Signal-Transduction Pathways 89
cAMP regulates transcription via the transcription factors CREB and CBP 89
Receptor tyrosine kinases regulate transcription via a Ras-dependent cascade of protein kinases 89
Tyrosine kinase–associated receptors can regulate transcription via JAK-STAT 90
Nuclear receptors are transcription factors 90
Modular Construction 90
Dimerization 90
Activation of Transcription 90
Repression of Transcription 92
Physiological stimuli can modulate transcription factors, which can coordinate complex cellular responses 92
Epigenetic Regulation of Gene Expression 94
Epigenetic regulation can result in long-term gene silencing 94
Alterations in chromatin structure may mediate epigenetic regulation, stimulating or inhibiting gene transcription 94
Histone methylation may stimulate or inhibit gene expression 94
DNA methylation is associated with gene inactivation 95
Post-Translational Regulation of Gene Expression 96
Alternative splicing generates diversity from single genes 96
Retained Intron 97
Alternative 3′ Splice Sites 97
Alternative 5′ Splice Sites 97
Cassette Exons 97
Mutually Exclusive Exons 97
Alternative 5′ Ends 98
Alternative 3′ Ends 98
Regulatory elements in the 3′ untranslated region control mRNA stability 98
MicroRNAs regulate mRNA abundance and translation 99
References 100
References 101.e1
Books and Reviews 101.e1
Journal Articles 101.e1
Glossary 100
5 Transport of Solutes and Water 102
The Intracellular and Extracellular Fluids 102
Total-body water is the sum of the ICF and ECF volumes 102
Plasma Volume 102
Interstitial Fluid 102
Transcellular Fluid 102
ICF is rich in K+, whereas ECF is rich in Na+ and Cl− 102
Volume Occupied by Plasma Proteins 103
Effect of Protein Charge 104
All body fluids have approximately the same osmolality, and each fluid has equal numbers of positive and negative charges 105
Osmolality 105
Electroneutrality 105
Solute Transport Across Cell Membranes 105
In passive, noncoupled transport across a permeable membrane, a solute moves down its electrochemical gradient 105
At equilibrium, the chemical and electrical potential energy differences across the membrane are equal but opposite 106
(Vm − EX) is the net electrochemical driving force acting on an ion 107
In simple diffusion, the flux of an uncharged substance through membrane lipid is directly proportional to its concentration difference 108
Some substances cross the membrane passively through intrinsic membrane proteins that can form pores, channels, or carriers 108
Water-filled pores can allow molecules, some as large as 45 kDa, to cross membranes passively 109
Gated channels, which alternately open and close, allow ions to cross the membrane passively 110
Na+ Channels 111
K+ Channels 111
Ca2+ Channels 111
Proton Channels 111
Anion Channels 111
Some carriers facilitate the passive diffusion of small solutes such as glucose 111
The physical structures of pores, channels, and carriers are quite similar 115
The Na-K pump, the most important primary active transporter in animal cells, uses the energy of ATP to extrude Na+ and take up K 115
Besides the Na-K pump, other P-type ATPases include the H-K and Ca pumps 117
H-K Pump 117
Ca Pumps 118
Other Pumps 118
The F-type and the V-type ATPases transport H 118
F-type or FoF1 ATPases 118
V-type H Pump 118
ATP-binding cassette transporters can act as pumps, channels, or regulators 119
ABCA Subfamily 119
MDR Subfamily 120
MRP/CFTR Subfamily 120
Cotransporters, one class of secondary active transporters, are generally driven by the energy of the inwardly directed Na+ gradient 120
Na/Glucose Cotransporter 121
Na+-Driven Cotransporters for Organic Solutes 122
Na/HCO3 Cotransporters 122
Na+-Driven Cotransporters for Other Inorganic Anions 122
Na/K/Cl Cotransporter 122
Na/Cl Cotransporter 123
K/Cl Cotransporter 123
H+-Driven Cotransporters 123
Exchangers, another class of secondary active transporters, exchange ions for one another 123
Na-Ca Exchanger 123
Na-H Exchanger 124
Na+-Driven Cl-HCO3 Exchanger 124
Cl-HCO3 Exchanger 124
Other Anion Exchangers 125
Regulation of Intracellular Ion Concentrations 125
The Na-K pump keeps [Na+] inside the cell low and [K+] high 125
The Ca pump and the Na-Ca exchanger keep intracellular [Ca2+] four orders of magnitude lower than extracellular [Ca2+] 126
Ca Pump (SERCA) in Organelle Membranes 126
Ca Pump (PMCA) on the Plasma Membrane 126
Na-Ca Exchanger (NCX) on the Plasma Membrane 126
In most cells, [Cl−] is modestly above equilibrium because Cl− uptake by the Cl-HCO3 exchanger and Na/K/Cl cotransporter balances passive Cl− efflux through channels 127
The Na-H exchanger and Na+-driven transporters keep the intracellular pH and [] above their equilibrium values 127
Water Transport and the Regulation of Cell Volume 127
Water transport is driven by osmotic and hydrostatic pressure differences across membranes 127
Because of the presence of impermeant, negatively charged proteins within the cell, Donnan forces will lead to cell swelling 128
The Na-K pump maintains cell volume by doing osmotic work that counteracts the passive Donnan forces 130
Cell volume changes trigger rapid changes in ion channels or transporters, returning volume toward normal 130
Response to Cell Shrinkage 131
Response to Cell Swelling 131
Cells respond to long-term hyperosmolality by accumulating new intracellular organic solutes 132
The gradient in tonicity—or effective osmolality—determines the osmotic flow of water across a cell membrane 132
Water Exchange Across Cell Membranes 132
Water Exchange Across the Capillary Wall 133
Adding isotonic saline, pure water, or pure NaCl to the ECF will increase ECF volume but will have divergent effects on ICF volume and ECF osmolality 134
Infusion of Isotonic Saline 135
Infusion of “Solute-Free” Water 135
Ingestion of Pure NaCl Salt 135
Whole-body Na+ content determines ECF volume, whereas whole-body water content determines osmolality 135
Transport of Solutes and Water Across Epithelia 136
The epithelial cell generally has different electrochemical gradients across its apical and basolateral membranes 136
Tight and leaky epithelia differ in the permeabilities of their tight junctions 136
Epithelial cells can absorb or secrete different solutes by inserting specific channels or transporters at either the apical or basolateral membrane 137
Na+ Absorption 137
K+ Secretion 138
Glucose Absorption 138
Cl− Secretion 139
Water transport across epithelia passively follows solute transport 139
Absorption of a Hyperosmotic Fluid 139
Absorption of an Isosmotic Fluid 139
Absorption of a Hypo-osmotic Fluid 139
Epithelia can regulate transport by controlling transport proteins, tight junctions, and the supply of the transported substances 139
Increased Synthesis (or Degradation) of Transport Proteins 139
Recruitment of Transport Proteins to the Cell Membrane 140
Post-translational Modification of Pre-existing Transport Proteins 140
Changes in the Paracellular Pathway 140
Luminal Supply of Transported Species and Flow Rate 140
References 140
References 140.e1
Books and Reviews 140.e1
Journal Articles 140.e2
6 Electrophysiology of the Cell Membrane 141
Ionic Basis of Membrane Potentials 141
Principles of electrostatics explain why aqueous pores formed by channel proteins are needed for ion diffusion across cell membranes 141
Membrane potentials can be measured with microelectrodes as well as dyes or fluorescent proteins that are voltage sensitive 143
Membrane potential is generated by ion gradients 144
For mammalian cells, Nernst potentials for ions typically range from −100 mV for K+ to +100 mV for Ca2 146
Currents carried by ions across membranes depend on the concentration of ions on both sides of the membrane, the membrane potential, and the permeability of the membrane to each ion 146
Membrane potential depends on ionic concentration gradients and permeabilities 148
Electrical Model of a Cell Membrane 149
The cell membrane model includes various ionic conductances and electromotive forces in parallel with a capacitor 149
The separation of relatively few charges across the bilayer capacitance maintains the membrane potential 150
Ionic current is directly proportional to the electrochemical driving force (Ohm’s law) 150
Capacitative current is proportional to the rate of voltage change 151
A voltage clamp measures currents across cell membranes 152
The patch-clamp technique resolves unitary currents through single channel molecules 154
Single channel currents sum to produce macroscopic membrane currents 154
Single channels can fluctuate between open and closed states 156
Molecular Physiology of Ion Channels 157
Classes of ion channels can be distinguished on the basis of electrophysiology, pharmacological and physiological ligands, intracellular messengers, and sequence homology 157
Electrophysiology 157
Pharmacological Ligands 158
Physiological Ligands 158
Intracellular Messengers 158
Sequence Homology 158
Many channels are formed by a radially symmetric arrangement of subunits or domains around a central pore 158
Gap junction channels are made up of two connexons, each of which has six identical subunits called connexins 158
An evolutionary tree called a dendrogram illustrates the relatedness of ion channels 159
Hydrophobic domains of channel proteins can predict how these proteins weave through the membrane 161
Protein superfamilies, subfamilies, and subtypes are the structural bases of channel diversity 162
Connexins 162
K+ Channels 162
HCN, CNG, and TRP Channels 162
NAADP Receptor 165
Voltage-Gated Na+ Channels 165
Voltage-Gated Ca2+ Channels 165
CatSper Channels 165
Hv Channels 165
Ligand-Gated Channels 165
Other Ion Channels 165
References 165
References 165.e2
Books and Reviews 165.e2
Journal Articles 165.e2
7 Electrical Excitability and Action Potentials 173
Mechanisms of Nerve and Muscle Action Potentials 173
An action potential is a transient depolarization triggered by a depolarization beyond a threshold 173
In contrast to an action potential, a graded response is proportional to stimulus intensity and decays with distance along the axon 174
Excitation of a nerve or muscle depends on the product (strength × duration) of the stimulus and on the refractory period 176
The action potential arises from changes in membrane conductance to Na+ and K 176
The Na+ and K+ currents that flow during the action potential are time and voltage dependent 177
Time Dependence of Na+ and K+ Currents 177
Voltage Dependence of Na+ and K+ Currents 178
Macroscopic Na+ and K+ currents result from the opening and closing of many channels 180
The Hodgkin-Huxley model predicts macroscopic currents and the shape of the action potential 181
Physiology of Voltage-Gated Channels and Their Relatives 182
A large superfamily of structurally related membrane proteins includes voltage-gated and related channels 182
Na+ channels generate the rapid initial depolarization of the action potential 185
Na+ channels are blocked by neurotoxins and local anesthetics 187
Ca2+ channels contribute to action potentials in some cells and also function in electrical and chemical coupling mechanisms 189
Ca2+ channels are characterized as L-, T-, P/Q-, N-, and R-type channels on the basis of kinetic properties and inhibitor sensitivity 190
K+ channels determine resting potential and regulate the frequency and termination of action potentials 193
The Kv (or Shaker-related) family of K+ channels mediates both the delayed outward-rectifier current and the transient A-type current 193
Two families of KCa K+ channels mediate Ca2+-activated K+ currents 196
The Kir K+ channels mediate inward-rectifier K+ currents, and K2P channels may sense stress 196
Propagation of Action Potentials 199
The propagation of electrical signals in the nervous system involves local current loops 199
Myelin improves the efficiency with which axons conduct action potentials 199
The cable properties of the membrane and cytoplasm determine the velocity of signal propagation 201
References 203
References 203.e1
Books and Reviews 203.e1
Journal Articles 203.e1
8 Synaptic Transmission and the Neuromuscular Junction 204
Mechanisms of Synaptic Transmission 204
Electrical continuity between cells is established by electrical or chemical synapses 204
Electrical synapses directly link the cytoplasm of adjacent cells 205
Chemical synapses use neurotransmitters to provide electrical continuity between adjacent cells 206
Neurotransmitters can activate ionotropic or metabotropic receptors 206
Synaptic Transmission at the Neuromuscular Junction 208
Neuromuscular junctions are specialized synapses between motor neurons and skeletal muscle 208
ACh activates nicotinic AChRs to produce an excitatory end-plate current 210
The nicotinic AChR is a member of the pentameric Cys-loop receptor family of ligand-gated ion channels 212
Activation of AChR channels requires binding of two ACh molecules 213
Miniature EPPs reveal the quantal nature of transmitter release from the presynaptic terminals 214
Direct sensing of extracellular transmitter also shows quantal release of transmitter 215
Synaptic vesicles package, store, and deliver neurotransmitters 217
Neurotransmitter release occurs by exocytosis of synaptic vesicles 219
Re-uptake or cleavage of the neurotransmitter terminates its action 221
Toxins and Drugs Affecting Synaptic Transmission 222
Guanidinium neurotoxins such as tetrodotoxin prevent depolarization of the nerve terminal, whereas dendrotoxins inhibit repolarization 222
ω-Conotoxin blocks Ca2+ channels that mediate Ca2+ influx into nerve terminals, inhibiting synaptic transmission 224
Bacterial toxins such as tetanus and botulinum toxins cleave proteins involved in exocytosis, preventing fusion of synaptic vesicles 224
Both agonists and antagonists of the nicotinic AChR can prevent synaptic transmission 225
Inhibitors of AChE prolong and magnify the EPP 226
References 227
References 227.e2
Books and Reviews 227.e2
Journal Articles 227.e2
9 Cellular Physiology of Skeletal, Cardiac, and Smooth Muscle 228
Skeletal Muscle 228
Contraction of skeletal muscle is initiated by motor neurons that innervate motor units 228
Action potentials propagate from the sarcolemma to the interior of muscle fibers along the transverse tubule network 229
Depolarization of the T-tubule membrane results in Ca2+ release from the SR at the triad 229
Striations of skeletal muscle fibers correspond to ordered arrays of thick and thin filaments within myofibrils 232
Thin and thick filaments are supramolecular assemblies of protein subunits 233
Thin Filaments 233
Thick Filaments 233
During the cross-bridge cycle, contractile proteins convert the energy of ATP hydrolysis into mechanical energy 234
An increase in [Ca2+]i triggers contraction by removing the inhibition of cross-bridge cycling 236
Termination of contraction requires re-uptake of Ca2+ into the SR 237
Muscle contractions produce force under isometric conditions and force with shortening under isotonic conditions 237
Muscle length influences tension development by determining the degree of overlap between actin and myosin filaments 238
At higher loads, the velocity of shortening is lower because more cross-bridges are simultaneously active 240
In a single skeletal muscle fiber, the force developed may be increased by summing multiple twitches in time 241
In a whole skeletal muscle, the force developed may be increased by summing the contractions of multiple fibers 241
Cardiac Muscle 242
Action potentials propagate between adjacent cardiac myocytes through gap junctions 242
Cardiac contraction requires Ca2+ entry through L-type Ca2+ channels 242
Cross-bridge cycling and termination of cardiac muscle contraction are similar to the events in skeletal muscle 243
In cardiac muscle, increasing the entry of Ca2+ enhances the contractile force 243
Smooth Muscle 243
Smooth muscles may contract in response to synaptic transmission or electrical coupling 243
Action potentials of smooth muscles may be brief or prolonged 244
Some smooth-muscle cells spontaneously generate either pacemaker currents or slow waves 244
Some smooth muscles contract without action potentials 246
In smooth muscle, both entry of extracellular Ca2+ and intracellular Ca2+ spark activate contraction 246
Ca2+ Entry via Voltage-Gated Channels 247
Ca2+ Release from the SR 247
Ca2+ Entry through Store-Operated Ca2+ Channels (SOCs) 247
Ca2+-dependent phosphorylation of the myosin regulatory light chain activates cross-bridge cycling in smooth muscle 247
Termination of smooth-muscle contraction requires dephosphorylation of myosin light chain 248
Smooth-muscle contraction may also occur independently of increases in [Ca2+]i 248
In smooth muscle, increases in both [Ca2+]i and the Ca2+ sensitivity of the contractile apparatus enhance contractile force 249
Smooth muscle maintains high force at low energy consumption 249
Diversity among Muscles 249
Skeletal muscle is composed of slow-twitch and fast-twitch fibers 249
The properties of cardiac cells vary with location in the heart 250
The properties of smooth-muscle cells differ markedly among tissues and may adapt with time 250
Smooth-muscle cells express a wide variety of neurotransmitter and hormone receptors 251
References 251
References 251.e1
Books and Reviews 251.e1
Journal Articles 251.e1
III The Nervous System 253
10 Organization of the Nervous System 254
The nervous system can be divided into central, peripheral, and autonomic nervous systems 254
Each area of the nervous system has unique nerve cells and a different function 254
Cells of the Nervous System 255
The neuron doctrine first asserted that the nervous system is composed of many individual signaling units—the neurons 255
Nerve cells have four specialized regions: cell body, dendrites, axon, and presynaptic terminals 255
Cell Body 255
Dendrites 255
Axon 255
Presynaptic Terminals 256
The cytoskeleton helps compartmentalize the neuron and also provides the tracks along which material travels between different parts of the neuron 257
Fast Axoplasmic Transport 257
Fast Retrograde Transport 259
Slow Axoplasmic Transport 259
Neurons can be classified on the basis of their axonal projection, their dendritic geometry, and the number of processes emanating from the cell body 259
Axonal Projection 259
Dendritic Geometry 259
Number of Processes 259
Glial cells provide a physiological environment for neurons 259
Development of Neurons and Glial Cells 261
Neurons differentiate from the neuroectoderm 261
Neurons and glial cells originate from cells in the proliferating germinal matrix near the ventricles 263
Neurons migrate to their correct anatomical position in the brain with the help of adhesion molecules 267
Neurons do not regenerate 267
Neurons 267
Axons 267
Glia 269
Subdivisions of the Nervous System 269
The CNS consists of the telencephalon, cerebellum, diencephalon, midbrain, pons, medulla, and spinal cord 269
Telencephalon 269
Cerebellum 270
Diencephalon 270
Brainstem (Midbrain, Pons, and Medulla) 270
Spinal Cord 271
The PNS comprises the cranial and spinal nerves, their associated sensory ganglia, and various sensory receptors 271
The ANS innervates effectors that are not under voluntary control 273
References 274
References 274.e1
Books and Reviews 274.e1
Journal Articles 274.e1
11 The Neuronal Microenvironment 275
Extracellular fluid in the brain provides a highly regulated environment for central nervous system neurons 275
The brain is physically and metabolically fragile 275
Cerebrospinal Fluid 275
CSF fills the ventricles and subarachnoid space 275
The brain floats in CSF, which acts as a shock absorber 278
The choroid plexuses secrete CSF into the ventricles, and the arachnoid granulations absorb it 278
The epithelial cells of the choroid plexus secrete the CSF 279
Brain Extracellular Space 282
Neurons, glia, and capillaries are packed tightly together in the CNS 282
The CSF communicates freely with the BECF, which stabilizes the composition of the neuronal microenvironment 282
The ion fluxes that accompany neural activity cause large changes in extracellular ion concentration 284
The Blood-Brain Barrier 284
The blood-brain barrier prevents some blood constituents from entering the brain extracellular space 284
Continuous tight junctions link brain capillary endothelial cells 285
Uncharged and lipid-soluble molecules more readily pass through the blood-brain barrier 286
Transport by capillary endothelial cells contributes to the blood-brain barrier 286
Glial Cells 287
Glial cells constitute half the volume of the brain and outnumber neurons 287
Astrocytes supply fuel to neurons in the form of lactic acid 287
Astrocytes are predominantly permeable to K+ and also help regulate [K+]o 289
Gap junctions couple astrocytes to one another, allowing diffusion of small solutes 289
Astrocytes synthesize neurotransmitters, take them up from the extracellular space, and have neurotransmitter receptors 290
Astrocytes secrete trophic factors that promote neuronal survival and synaptogenesis 292
Astrocytic endfeet modulate cerebral blood flow 292
Oligodendrocytes and Schwann cells make and sustain myelin 292
Oligodendrocytes are involved in pH regulation and iron metabolism in the brain 293
Microglial cells are the macrophages of the CNS 294
References 294
References 294.e1
Books and Reviews 294.e1
Journal Articles 294.e1
12 Physiology of Neurons 295
Neurons receive, combine, transform, store, and send information 295
Neural information flows from dendrite to soma to axon to synapse 295
Signal Conduction in Dendrites 297
Dendrites attenuate synaptic potentials 297
Dendritic membranes have voltage-gated ion channels 299
Control of Spiking Patterns in the Soma 300
Neurons can transform a simple input into a variety of output patterns 300
Intrinsic firing patterns are determined by a variety of ion currents with relatively slow kinetics 301
Axonal Conduction 301
Axons are specialized for rapid, reliable, and efficient transmission of electrical signals 301
Action potentials are usually initiated at the initial segment 302
Conduction velocity of a myelinated axon increases linearly with diameter 302
Demyelinated axons conduct action potentials slowly, unreliably, or not at all 304
References 306
References 306.e1
Books and Reviews 306.e1
Journal Articles 306.e1
13 Synaptic Transmission in the Nervous System 307
Neuronal Synapses 307
The molecular mechanisms of neuronal synapses are similar but not identical to those of the neuromuscular junction 307
Presynaptic terminals may contact neurons at the dendrite, soma, or axon and may contain both clear vesicles and dense-core granules 309
The postsynaptic membrane contains transmitter receptors and numerous proteins clustered in the postsynaptic density 310
Some transmitters are used by diffusely distributed systems of neurons to modulate the general excitability of the brain 311
Electrical synapses serve specialized functions in the mammalian nervous system 314
Neurotransmitter Systems of the Brain 314
Most of the brain’s transmitters are common biochemicals 315
Synaptic transmitters can stimulate, inhibit, or modulate the postsynaptic neuron 318
Excitatory Synapses 318
Inhibitory Synapses 319
Modulatory Synapses 319
G proteins may affect ion channels directly, or indirectly through second messengers 320
Signaling cascades allow amplification, regulation, and a long duration of transmitter responses 321
Neurotransmitters may have both convergent and divergent effects 322
Fast Amino Acid–Mediated Synapses in the CNS 322
Most EPSPs in the brain are mediated by two types of glutamate-gated channels 323
Most IPSPs in the brain are mediated by the GABAA receptor, which is activated by several classes of drugs 325
The ionotropic receptors for ACh, serotonin, GABA, and glycine belong to the superfamily of ligand-gated/pentameric channels 326
Most neuronal synapses release a very small number of transmitter quanta with each action potential 327
When multiple transmitters colocalize to the same synapse, the exocytosis of large vesicles requires high-frequency stimulation 327
Plasticity of Central Synapses 328
Use-dependent changes in synaptic strength underlie many forms of learning 328
Short-term synaptic plasticity usually reflects presynaptic changes 328
Long-term potentiation in the hippocampus may last for days or weeks 329
Long-term depression exists in multiple forms 331
Long-term depression in the cerebellum may be important for motor learning 331
References 333
References 333.e1
Books and Reviews 333.e1
Journal Articles 333.e1
14 The Autonomic Nervous System 334
Organization of the Visceral Control System 334
The ANS has sympathetic, parasympathetic, and enteric divisions 334
Sympathetic preganglionic neurons originate from spinal segments T1 to L3 and synapse with postganglionic neurons in paravertebral or prevertebral ganglia 335
Preganglionic Neurons 335
Paravertebral Ganglia 335
Prevertebral Ganglia 336
Postganglionic Neurons 336
Cranial Nerves III, VII, and IX 338
Cranial Nerve X 339
Sacral Nerves 339
The visceral control system also has an important afferent limb 339
The enteric division is a self-contained nervous system of the GI tract and receives sympathetic and parasympathetic input 339
Synaptic Physiology of the Autonomic Nervous System 340
The sympathetic and parasympathetic divisions have opposite effects on most visceral targets 340
All preganglionic neurons—both sympathetic and parasympathetic—release acetylcholine and stimulate N2 nicotinic receptors on postganglionic neurons 341
All postganglionic parasympathetic neurons release ACh and stimulate muscarinic receptors on visceral targets 341
Most postganglionic sympathetic neurons release norepinephrine onto visceral targets 342
Postganglionic sympathetic and parasympathetic neurons often have muscarinic as well as nicotinic receptors 343
Nonclassic transmitters can be released at each level of the ANS 344
Two of the most unusual nonclassic neurotransmitters, ATP and nitric oxide, were first identified in the ANS 345
ATP 346
Nitric Oxide 346
Central Nervous System Control of the Viscera 347
Sympathetic output can be massive and nonspecific, as in the fight-or-flight response, or selective for specific target organs 347
Parasympathetic neurons participate in many simple involuntary reflexes 348
A variety of brainstem nuclei provide basic control of the ANS 348
The forebrain can modulate autonomic output, and reciprocally, visceral sensory input integrated in the brainstem can influence or even overwhelm the forebrain 348
CNS control centers oversee visceral feedback loops and orchestrate a feed-forward response to meet anticipated needs 349
The ANS has multiple levels of reflex loops 350
References 352
References 352.e1
Books and Reviews 352.e1
Journal Articles 352.e1
15 Sensory Transduction 353
Sensory receptors convert environmental energy into neural signals 353
Sensory transduction uses adaptations of common molecular signaling mechanisms 353
Sensory transduction requires detection and amplification, usually followed by a local receptor potential 353
Chemoreception 354
Chemoreceptors are ubiquitous, diverse, and evolutionarily ancient 354
Taste receptors are modified epithelial cells, whereas olfactory receptors are neurons 354
Taste Receptor Cells 354
Olfactory Receptor Cells 354
Complex flavors are derived from a few basic types of taste receptors, with contributions from sensory receptors of smell, temperature, texture, and pain 356
Taste transduction involves many types of molecular signaling systems 356
Salty 357
Sour 357
Sweet 358
Bitter 358
Amino Acids 358
Olfactory transduction involves specific receptors, G protein–coupled signaling, and a cyclic nucleotide–gated ion channel 358
Visual Transduction 359
The optical components of the eye collect light and focus it onto the retina 360
The retina is a small, displaced part of the CNS 363
There are three primary types of photoreceptors: rods, cones, and intrinsically photosensitive ganglion cells 363
Rods and cones hyperpolarize in response to light 365
Rhodopsin is a G protein–coupled “receptor” for light 367
The eye uses a variety of mechanisms to adapt to a wide range of light levels 368
Color vision depends on the different spectral sensitivities of the three types of cones 369
The ipRGCs have unique properties and functions 370
Vestibular and Auditory Transduction: Hair Cells 371
Bending the stereovilli of hair cells along one axis causes cation channels to open or to close 372
The otolithic organs (saccule and utricle) detect the orientation and linear acceleration of the head 374
The semicircular canals detect the angular acceleration of the head 375
The outer and middle ears collect and condition air pressure waves for transduction within the inner ear 376
Outer Ear 376
Middle Ear 376
The cochlea is a spiral of three parallel, fluid-filled tubes 377
Inner hair cells transduce sound, whereas the active movements of outer hair cells amplify the signal 378
The frequency sensitivity of auditory hair cells depends on their position along the basilar membrane of the cochlea 380
Somatic Sensory Receptors, Proprioception, and Pain 383
A variety of sensory endings in the skin transduce mechanical, thermal, and chemical stimuli 383
Mechanoreceptors in the skin provide sensitivity to specific stimuli such as vibration and steady pressure 383
Separate thermoreceptors detect warmth and cold 385
Nociceptors are specialized sensory endings that transduce painful stimuli 387
Muscle spindles sense changes in the length of skeletal muscle fibers, whereas Golgi tendon organs gauge the muscle’s force 388
References 389
References 389.e1
Books and Reviews 389.e1
Journal Articles 389.e1
16 Circuits of the Central Nervous System 390
Elements of Neural Circuits 390
Neural circuits process sensory information, generate motor output, and create spontaneous activity 390
Nervous systems have several levels of organization 390
Most local circuits have three elements: input axons, interneurons, and projection (output) neurons 391
Simple, Stereotyped Responses: Spinal Reflex Circuits 392
Passive stretching of a skeletal muscle causes a reflexive contraction of that same muscle and relaxation of the antagonist muscles 392
Force applied to the Golgi tendon organ regulates muscle contractile strength 394
Noxious stimuli can evoke complex reflexive movements 394
Spinal reflexes are strongly influenced by control centers within the brain 394
Rhythmic Activity: Central Pattern Generators 396
Central pattern generators in the spinal cord can create a complex motor program even without sensory feedback 396
Pacemaker cells and synaptic interconnections both contribute to central pattern generation 397
Central pattern generators in the spinal cord take advantage of sensory feedback, interconnections among spinal segments, and interactions with brainstem control centers 398
Spatial Representations: Sensory and Motor Maps in the Brain 399
The nervous system contains maps of sensory and motor information 399
The cerebral cortex has multiple visuotopic maps 399
Maps of somatic sensory information magnify some parts of the body more than others 400
The cerebral cortex has a motor map that is adjacent to and well aligned with the somatosensory map 402
Sensory and motor maps are fuzzy and plastic 403
Temporal Representations: Time-Measuring Circuits 405
To localize sound, the brain compares the timing and intensity of input to the ears 405
The brain measures interaural timing by a combination of neural delay lines and coincidence detectors 405
References 407
References 407.e1
Books and Reviews 407.e1
Journal Articles 407.e1
IV The Cardiovascular System 409
17 Organization of the Cardiovascular System 410
Elements of the Cardiovascular System 410
The circulation is an evolutionary consequence of body size 410
The heart is a dual pump that drives the blood in two serial circuits: the systemic and the pulmonary circulations 410
Hemodynamics 412
Blood flow is driven by a constant pressure head across variable resistances 412
Blood pressure is always measured as a pressure difference between two points 412
Total blood flow, or cardiac output, is the product (heart rate) × (stroke volume) 414
Flow in an idealized vessel increases with the fourth power of radius (Poiseuille equation) 415
Viscous resistance to flow is proportional to the viscosity of blood but does not depend on properties of the blood vessel walls 415
The viscosity of blood is a measure of the internal slipperiness between layers of fluid 415
How Blood Flows 416
Blood flow is laminar 416
Pressure and flow oscillate with each heartbeat between maximum systolic and minimum diastolic values 417
Origins of Pressure in the Circulation 418
Gravity causes a hydrostatic pressure difference when there is a difference in height 418
Low compliance of a vessel causes the transmural pressure to increase when the vessel blood volume is increased 419
The viscous resistance of blood causes an axial pressure difference when there is flow 419
The inertia of the blood and vessels causes pressure to decrease when the velocity of blood flow increases 420
How to Measure Blood Pressure, Blood Flow, and Cardiac Volumes 420
Blood pressure can be measured directly by puncturing the vessel 420
Blood pressure can be measured indirectly by use of a sphygmomanometer 421
Blood flow can be measured directly by electromagnetic and ultrasound flowmeters 422
Invasive Methods 422
Noninvasive Methods 423
Cardiac output can be measured indirectly by the Fick method, which is based on the conservation of mass 423
Cardiac output can be measured indirectly by dilution methods 424
Regional blood flow can be measured indirectly by “clearance” methods 426
Ventricular dimensions, ventricular volumes, and volume changes can be measured by angiography and echocardiography 426
References 428
References 428.e2
Books and Reviews 428.e2
Journal Articles 428.e2
18 Blood 429
Blood Composition 429
Whole blood is a suspension of cellular elements in plasma 429
Bone marrow is the source of most blood cells 431
RBCs are mainly composed of hemoglobin 434
Leukocytes defend against infections 435
Neutrophils 435
Eosinophils 435
Basophils 435
Lymphocytes 435
Monocytes 435
Platelets are nucleus-free fragments 435
Blood Viscosity 436
Whole blood has an anomalous viscosity 436
Blood viscosity increases with the hematocrit and the fibrinogen plasma concentration 437
Fibrinogen 437
Hematocrit 437
Vessel Radius 437
Velocity of Flow 438
Temperature 438
Hemostasis and Fibrinolysis 439
Platelets can plug holes in small vessels 439
Adhesion 439
Activation 440
Aggregation 440
A controlled cascade of proteolysis creates a blood clot 440
Intrinsic Pathway (Surface Contact Activation) 442
Extrinsic Pathway (Tissue Factor Activation) 442
Common Pathway 442
Coagulation as a Connected Diagram 444
Anticoagulants keep the clotting network in check 444
Paracrine Factors 444
Anticoagulant Factors 444
Fibrinolysis breaks up clots 445
References 446
References 446.e1
Books and Reviews 446.e1
Journal Articles 446.e1
19 Arteries and Veins 447
Arterial Distribution and Venous Collection Systems 447
Physical properties of vessels closely follow the level of branching in the circuit 447
Most of the blood volume resides in the systemic veins 448
The intravascular pressures along the systemic circuit are higher than those along the pulmonary circuit 450
Under normal conditions, the steepest pressure drop in the systemic circulation occurs in arterioles, the site of greatest vascular resistance 451
Local intravascular pressure depends on the distribution of vascular resistance 451
Elastic Properties of Blood Vessels 452
Blood vessels are elastic tubes 452
Because of the elastic properties of vessels, the pressure-flow relationship of passive vascular beds is nonlinear 453
Contraction of smooth muscle halts blood flow when driving pressure falls below the critical closing pressure 454
Elastic and collagen fibers determine the distensibility and compliance of vessels 454
Differences in compliance cause arteries to act as resistors and veins to act as capacitors 455
Laplace’s law describes how tension in the vessel wall increases with transmural pressure 455
The vascular wall is adapted to withstand wall tension, not transmural pressure 457
Elastin and collagen separately contribute to the wall tension of vessels 458
Aging reduces the distensibility of arteries 458
Active tension from smooth-muscle activity adds to the elastic tension of vessels 459
Elastic tension helps stabilize vessels under vasomotor control 460
References 460
References 460.e1
Books and Reviews 460.e1
Journal Articles 460.e1
20 The Microcirculation 461
The microcirculation serves both nutritional and non-nutritional roles 461
The microcirculation extends from the arterioles to the venules 461
Capillary Exchange of Solutes 463
The exchange of O2 and CO2 across capillaries depends on the diffusional properties of the surrounding tissue 463
The O2 extraction ratio of a whole organ depends primarily on blood flow and metabolic demand 464
According to Fick’s law, the diffusion of small water-soluble solutes across a capillary wall depends on both the permeability and the concentration gradient 464
The whole-organ extraction ratio for small hydrophilic solutes provides an estimate of the solute permeability of capillaries 465
Small polar molecules have a relatively low permeability because they can traverse the capillary wall only by diffusing through water-filled pores (small-pore effect) 466
The exchange of macromolecules across capillaries can occur by transcytosis (large-pore effect) 467
Capillary Exchange of Water 467
Fluid transfer across capillaries is convective and depends on net hydrostatic and osmotic forces (i.e., Starling forces) 467
Capillary blood pressure (Pc) falls from ~35 mm Hg at the arteriolar end to ~15 mm Hg at the venular end 469
Arteriolar (Pa) and Venular (Pv) Pressure 469
Location 469
Time 469
Gravity 469
Interstitial fluid pressure (Pif) is slightly negative, except in encapsulated organs 469
Capillary colloid osmotic pressure (πc), which reflects the presence of plasma proteins, is ~25 mm Hg 470
Interstitial fluid colloid osmotic pressure (πif) varies between 0 and 10 mm Hg among different organs 470
The Starling principle predicts ultrafiltration at the arteriolar end and absorption at the venular end of most capillary beds 471
For continuous capillaries, the endothelial barrier for fluid exchange is more complex than considered by Starling 472
Lymphatics 474
Lymphatics return excess interstitial fluid to the blood 474
Flow in Initial Lymphatics 475
Flow in Collecting Lymphatics 475
Transport of Proteins and Cells 475
The circulation of extracellular fluids involves three convective loops: blood, interstitial fluid, and lymph 476
Regulation of the Microcirculation 477
The active contraction of vascular smooth muscle regulates precapillary resistance, which controls capillary blood flow 477
Contraction of Vascular Smooth Muscle 477
Relaxation of Vascular Smooth Muscle 477
Tissue metabolites regulate local blood flow in specific vascular beds, independently of the systemic regulation 477
The endothelium of capillary beds is the source of several vasoactive compounds, including nitric oxide, endothelium-derived hyperpolarizing factor, and endothelin 480
Nitric Oxide 480
Endothelium-Derived Hyperpolarizing Factor 480
Prostacyclin (Prostaglandin I2) 480
Endothelins 480
Thromboxane A2 480
Other Endothelial Factors 481
Autoregulation stabilizes blood flow despite large fluctuations in systemic arterial pressure 481
Blood vessels proliferate in response to growth factors by a process known as angiogenesis 481
Promoters of Vessel Growth 481
Inhibitors of Vessel Growth 482
References 482
References 482.e2
Books and Reviews 482.e2
Journal Articles 482.e2
21 Cardiac Electrophysiology and the Electrocardiogram 483
Electrophysiology of Cardiac Cells 483
The cardiac action potential starts in specialized muscle cells of the sinoatrial node and then propagates in an orderly fashion throughout the heart 483
The cardiac action potential conducts from cell to cell via gap junctions 483
Cardiac action potentials have as many as five distinctive phases 484
The Na+ current is the largest current in the heart 485
The Ca2+ current in the heart passes primarily through L-type Ca2+ channels 488
The repolarizing K+ current turns on slowly 488
Early Outward K+ Current (A-type Current) 488
G Protein–Activated K+ Current 488
KATP Current 488
The If current is mediated by a nonselective cation channel 488
Different cardiac tissues uniquely combine ionic currents to produce distinctive action potentials 488
The SA node is the primary pacemaker of the heart 489
The Concept of Pacemaker Activity 489
SA Node 489
AV Node 489
Purkinje Fibers 490
Atrial and ventricular myocytes fire action potentials but do not have pacemaker activity 490
Atrial Muscle 490
Ventricular Muscle 490
Acetylcholine and catecholamines modulate pacemaker activity, conduction velocity, and contractility 491
Acetylcholine 492
Catecholamines 492
The Electrocardiogram 493
An ECG generally includes five waves 493
A pair of ECG electrodes defines a lead 493
The Limb Leads 494
The Precordial Leads 494
A simple two-cell model can explain how a simple ECG can arise 496
Cardiac Arrhythmias 496
Conduction abnormalities are a major cause of arrhythmias 497
Partial (or Incomplete) Conduction Block 502
Complete Conduction Block 502
Re-Entry 502
Accessory Conduction Pathways 504
Fibrillation 505
Altered automaticity can originate from the sinus node or from an ectopic locus 505
Depolarization-Dependent Triggered Activity 505
Long QT Syndrome 506
Ca2+ overload and metabolic changes can also cause arrhythmias 506
Ca2+ Overload 506
Metabolism-Dependent Conduction Changes 506
Electromechanical Dissociation 506
References 506
References 506.e1
Books and Reviews 506.e1
Journal Articles 506.e1
22 The Heart as a Pump 507
The Cardiac Cycle 507
The closing and opening of the cardiac valves define four phases of the cardiac cycle 507
Changes in ventricular volume, pressure, and flow accompany the four phases of the cardiac cycle N22-1 508
Diastasis Period (Middle of Phase 1) 508
Atrial Contraction (End of Phase 1) 508
Isovolumetric Contraction (Phase 2) 508
Ejection or Outflow (Phase 3) 509
Isovolumetric Relaxation (Phase 4) 509
Rapid Ventricular Filling Period (Beginning of Phase 1) 510
The ECG, phonocardiogram, and echocardiogram all follow the cyclic pattern of the cardiac cycle 510
Aortic Blood Flow 510
Jugular Venous Pulse 510
Electrocardiogram 510
Phonocardiogram and Heart Sounds 511
Echocardiogram 511
The cardiac cycle causes flow waves in the aorta and peripheral vessels 511
Aortic Arch 513
Thoracic-Abdominal Aorta and Large Arteries 513
The cardiac cycle also causes pressure waves in the aorta and peripheral vessels 513
Terminal Arteries and Arterioles 513
Capillaries 513
Distortion of pressure waves is the result of their propagation along the arterial tree 513
Effect of Frequency on Wave Velocity and Damping 515
Effect of Wall Stiffness on Wave Velocity 515
Pressure waves in veins do not originate from arterial waves 515
Effect of the Cardiac Cycle 516
Effect of the Respiratory Cycle 516
Effect of Skeletal Muscle Contraction (“Muscle Pump”) 516
Cardiac Dynamics 517
The right ventricle contracts like a bellows, whereas the left ventricle contracts like a hand squeezing a tube of toothpaste 517
The right atrium contracts before the left, but the left ventricle contracts before the right 517
Atrial Contraction 517
Initiation of Ventricular Contraction 517
Ventricular Ejection 517
Ventricular Relaxation 519
Measurements of ventricular volumes, pressures, and flows allow clinicians to judge cardiac performance 519
Definitions of Cardiac Volumes 519
Measurements of Cardiac Volumes 519
Measurement of Ventricular Pressures 519
Measurement of Flows 519
The pressure-volume loop of a ventricle illustrates the ejection work of the ventricle 519
Segment AB 520
Segment BC 520
Segment CD 520
Segment DE 520
Segment EF 520
Segment FA 520
The “pumping work” done by the heart accounts for a small fraction of the total energy the heart consumes 520
From Contractile Filaments to a Regulated Pump 522
The entry of Ca2+ from the outside triggers Ca2+-induced Ca2+ release from the sarcoplasmic reticulum 522
A global rise in [Ca2+]i initiates contraction of cardiac myocytes 522
Phosphorylation of phospholamban and of troponin I speeds cardiac muscle relaxation 522
Extrusion of Ca2+ into the ECF 523
Reuptake of Ca2+ by the SR 523
Uptake of Ca2+ by Mitochondria 524
Dissociation of Ca2+ from Troponin C 524
The overlap of thick and thin filaments cannot explain the unusual shape of the cardiac length-tension diagram 524
Starling’s law states that a greater fiber length (i.e., greater ventricular volume) causes the heart to deliver more mechanical energy 524
The velocity of cardiac muscle shortening falls when the contraction occurs against a greater opposing force (or pressure) or at a shorter muscle length (or lower volume) 526
Increases in heart rate enhance myocardial tension 528
Contractility is an intrinsic measure of cardiac performance 528
Effect of Changes in Contractility 530
Effect of Changes in Preload (i.e., Initial Sarcomere Length) 530
Effect of Changes in Afterload 530
Positive inotropic agents increase myocardial contractility by raising [Ca2+]i 530
Positive Inotropic Agents 530
Negative Inotropic Agents 530
References 532
References 532.e1
Books and Reviews 532.e1
Journal Articles 532.e1
23 Regulation of Arterial Pressure and Cardiac Output 533
Short-Term Regulation of Arterial Pressure 533
Systemic mean arterial blood pressure is the principal variable that the cardiovascular system controls 533
Neural reflexes mediate the short-term regulation of mean arterial blood pressure 533
High-pressure baroreceptors at the carotid sinus and aortic arch are stretch receptors that sense changes in arterial pressure 534
Increased arterial pressure raises the firing rate of afferent baroreceptor nerves 536
The medulla coordinates afferent baroreceptor signals 537
The efferent pathways of the baroreceptor response include both sympathetic and parasympathetic divisions of the autonomic nervous system 537
Sympathetic Efferents 537
Parasympathetic Efferents 539
The principal effectors in the neural control of arterial pressure are the heart, the arteries, the veins, and the adrenal medulla 539
Sympathetic Input to the Heart (Cardiac Nerves) 539
Parasympathetic Input to the Heart (Vagus Nerve) 539
Sympathetic Input to Blood Vessels (Vasoconstrictor Response) 539
Parasympathetic Input to Blood Vessels (Vasodilator Response) 539
Sympathetic Input to Blood Vessels in Skeletal Muscle (Vasodilator Response) 539
Adrenal Medulla 539
The unique combination of agonists and receptors determines the end response in cardiac and vascular effector cells 542
Adrenergic Receptors in the Heart 542
Cholinergic Receptors in the Heart 542
Adrenergic Receptors in Blood Vessels 542
Cholinergic Receptors in or near Blood Vessels 543
Nonadrenergic, Noncholinergic Receptors in Blood Vessels 543
The medullary cardiovascular center tonically maintains blood pressure and is under the control of higher brain centers 543
Secondary neural regulation of arterial blood pressure depends on chemoreceptors 544
Carotid Bodies 545
Aortic Bodies 545
Afferent Fiber Input to the Medulla 545
Physiological Role of the Peripheral Chemoreceptors in Cardiovascular Control 545
Central Chemoreceptors 545
Regulation of Cardiac Output 545
Mechanisms intrinsic to the heart modulate both heart rate and stroke volume 545
Intrinsic Control of Heart Rate 545
Intrinsic Control of Stroke Volume 545
Mechanisms extrinsic to the heart also modulate heart rate and stroke volume 546
Baroreceptor Regulation 546
Chemoreceptor Regulation 546
Low-pressure baroreceptors in the atria respond to increased “fullness” of the vascular system, triggering tachycardia, renal vasodilation, and diuresis 546
Atrial Receptors 546
Ventricular Receptors 547
Cardiac output is roughly proportional to effective circulating blood volume 547
Matching of Venous Return and Cardiac Output 548
Increases in cardiac output cause right atrial pressure to fall 549
Changes in blood volume shift the vascular function curve to different RAPs, whereas changes in arteriolar tone alter the slope of the curve 550
Because vascular function and cardiac function depend on each other, cardiac output and venous return match at exactly one value of RAP 551
Intermediate- and Long-Term Control of the Circulation 551
Endocrine and paracrine vasoactive compounds control the circulatory system on an intermediate- to long-term basis 551
Biogenic Amines 553
Peptides 553
Prostaglandins 554
Nitric Oxide 554
Pathways for the renal control of ECF volume are the primary long-term regulators of mean arterial pressure 554
References 555
References 555.e1
Books and Reviews 555.e1
Journal Articles 555.e1
24 Special Circulations 556
The blood flow to individual organs must vary to meet the needs of the particular organ, as well as of the whole body 556
Neural, myogenic, metabolic, and endothelial mechanisms control regional blood flow 556
Neural Mechanisms 556
Myogenic Mechanisms 556
Metabolic Mechanisms 556
Endothelial Mechanisms 556
The Brain 557
Anastomoses at the circle of Willis and among the branches of distributing arteries protect the blood supply to the brain, which is ~15% of resting cardiac output 557
Arteries 557
Veins 557
Capillaries 558
Lymphatics 558
Vascular Volume 558
Neural, metabolic, and myogenic mechanisms control blood flow to the brain 558
Neural Control 558
Metabolic Control 559
Myogenic Control 559
The neurovascular unit matches blood flow to local brain activity 559
Autoregulation maintains a fairly constant cerebral blood flow across a broad range of perfusion pressures 559
The Heart 560
The coronary circulation receives 5% of the resting cardiac output from the left heart and mostly returns it to the right heart 560
Extravascular compression impairs coronary blood flow during systole 560
Myocardial blood flow parallels myocardial metabolism 561
Although sympathetic stimulation directly constricts coronary vessels, accompanying metabolic effects predominate, producing an overall vasodilation 562
Collateral vessel growth can provide blood flow to ischemic regions 562
Vasodilator drugs may compromise myocardial flow through “coronary steal” 562
The Skeletal Muscle 562
A microvascular unit is the capillary bed supplied by a single terminal arteriole 562
Metabolites released by active muscle trigger vasodilation and an increase in blood flow 563
Sympathetic innervation increases the intrinsic tone of resistance vessels 564
Rhythmic contraction promotes blood flow through the “muscle pump” 565
The Splanchnic Organs 565
The vascular supply to the gut is highly interconnected 565
Blood flow to the gastrointestinal tract increases up to eight-fold after a meal (postprandial hyperemia) 567
Sympathetic activity directly constricts splanchnic blood vessels, whereas parasympathetic activity indirectly dilates them 567
Changes in the splanchnic circulation regulate total peripheral resistance and the distribution of blood volume 568
Exercise and hemorrhage can substantially reduce splanchnic blood flow 568
The liver receives its blood flow from both the systemic and the portal circulation 568
The Skin 569
The skin is the largest organ of the body 569
Specialized arteriovenous anastomoses in apical skin help control heat loss 570
Apical Skin 570
Nonapical Skin 571
Mechanical stimuli elicit local vascular responses in the skin 571
White Reaction 571
“Triple Response” 571
References 571
References 571.e1
Books and Reviews 571.e1
Journal Articles 571.e1
25 Integrated Control of the Cardiovascular System 572
Interaction among the Different Cardiovascular Control Systems 572
The control of the cardiovascular system involves “linear,” “branched,” and “connected” interactions 572
Regulation of the entire cardiovascular system depends on the integrated action of multiple subsystem controls as well as noncardiovascular controls 572
Response to Erect Posture 575
Because of gravity, standing up (orthostasis) tends to shift blood from the head and heart to veins in the legs 575
The ANS mediates an “orthostatic response” that raises heart rate and peripheral vascular resistance and thus tends to restore mean arterial pressure 576
Nonuniform Initial Distribution of Blood 576
Nonuniform Distensibility of the Vessels 576
Muscle Pumps 576
Autonomic Reflexes 576
Postural Hypotension 576
Temperature Effects 576
Responses to Acute Emotional Stress 577
The fight-or-flight reaction is a sympathetic response that is centrally controlled in the cortex and hypothalamus 577
The common faint reflects mainly a parasympathetic response caused by sudden emotional stress 579
Response to Exercise 580
Early physiologists suggested that muscle contraction leads to mechanical and chemical changes that trigger an increase in cardiac output 580
Mechanical Response: Increased Venous Return 580
Chemical Response: Local Vasodilation in Active Muscle 580
Central command organizes an integrated cardiovascular response to exercise 581
Muscle and baroreceptor reflexes, metabolites, venous return, histamine, epinephrine, and increased temperature reinforce the response to exercise 581
Response to Hemorrhage 583
After hemorrhage, cardiovascular reflexes restore mean arterial pressure 583
Tachycardia and Increased Contractility 585
Arteriolar Constriction 585
Venous Constriction 585
Circulating Vasoactive Agonists 585
After hemorrhage, transcapillary refill, fluid conservation, and thirst restore the blood volume 585
Transcapillary Refill 585
Renal Conservation of Salt and Water 586
Thirst 586
Positive-feedback mechanisms cause irreversible hemorrhagic shock 587
Failure of the Vasoconstrictor Response 587
Failure of the Capillary Refill 587
Failure of the Heart 587
CNS Depression 587
References 587
References 587.e1
Books and Reviews 587.e1
Journal Articles 587.e1
V The Respiratory System 589
26 Organization of the Respiratory System 590
Comparative Physiology of Respiration 590
External respiration is the exchange of O2 and CO2 between the atmosphere and the mitochondria 590
Diffusion is the major mechanism of external respiration for small aquatic organisms 590
Convection enhances diffusion by producing steeper gradients across the diffusion barrier 592
Surface area amplification enhances diffusion 595
Respiratory pigments such as hemoglobin increase the carrying capacity of the blood for both O2 and CO2 595
Pathophysiology recapitulates phylogeny … in reverse 595
Organization of the Respiratory System in Humans 596
Humans optimize each aspect of external respiration—ventilation, circulation, area amplification, gas carriage, local control, and central control 596
Conducting airways deliver fresh air to the alveolar spaces 597
Alveolar air spaces are the site of gas exchange 597
The lungs play important nonrespiratory roles, including filtering the blood, serving as a reservoir for the left ventricle, and performing several biochemical conversions 600
Olfaction 600
Processing of Inhaled Air Before It Reaches the Alveoli 600
Left Ventricular Reservoir 600
Filtering Small Emboli from the Blood 600
Biochemical Reactions 600
Lung Volumes and Capacities 601
The spirometer measures changes in lung volume 601
The volume of distribution of helium or nitrogen in the lung is an estimate of the RV 602
Helium-Dilution Technique 602
N2-Washout Method 604
The plethysmograph, together with Boyle’s law, is a tool for estimation of RV 604
References 605
References 605.e1
Books and Reviews 605.e1
Journal Articles 605.e1
27 Mechanics of Ventilation 606
Static Properties of the Lung 606
The balance between the outward elastic recoil of the chest wall and the inward elastic recoil of the lungs generates a subatmospheric intrapleural pressure 606
Contraction of the diaphragm and selected intercostal muscles increases the volume of the thorax, producing an inspiration 606
Relaxation of the muscles of inspiration produces a quiet expiration 607
An increase of the static compliance makes it easier to inflate the lungs 608
Surface tension at the air-water interface of the airways accounts for most of the elastic recoil of the lungs 610
Pulmonary surfactant is a mixture of lipids—mainly dipalmitoylphosphatidylcholine—and apoproteins 613
Pulmonary surfactant reduces surface tension and increases compliance 615
Dynamic Properties of the Lung 616
Airflow is proportional to the difference between alveolar and atmospheric pressure, but inversely proportional to airway resistance 616
In the lung, airflow is transitional in most of the tracheobronchial tree 617
The smallest airways contribute only slightly to total airway resistance in healthy lungs 617
Vagal tone, histamine, and reduced lung volume all increase airway resistance 620
Intrapleural pressure has a static component (−PTP) that determines lung volume and a dynamic component (Pa) that determines airflow 620
Transpulmonary Pressure 621
Alveolar Pressure 621
During inspiration, a sustained negative shift in PIP causes Pa to become transiently more negative 622
Dynamic compliance falls as respiratory frequency rises 622
Transmural pressure differences cause airways to dilate during inspiration and to compress during expiration 624
Static Conditions 625
Inspiration 625
Expiration 626
Because of airway collapse, expiratory flow rates become independent of effort at low lung volumes 626
References 627
References 627.e1
Books and Reviews 627.e1
Journal Articles 627.e1
28 Acid-Base Physiology 628
pH and Buffers 628
pH values vary enormously among different intracellular and extracellular compartments 628
Buffers minimize the size of the pH changes produced by adding acid or alkali to a solution 628
According to the Henderson-Hasselbalch equation, pH depends on the ratio [CO2]/[] 629
has a far higher buffering power in an open than in a closed system 630
Acid-Base Chemistry When Is the Only Buffer 633
In the absence of other buffers, doubling causes pH to fall by 0.3 but causes almost no change in [] 633
In the absence of other buffers, doubling [] causes pH to rise by 0.3 634
Acid-Base Chemistry in the Presence of and Buffers—The Davenport Diagram 635
The Davenport diagram is a graphical tool for interpreting acid-base disturbances in blood 635
The Buffer 635
Buffers 636
Solving the Problem 637
The amount of formed or consumed during “respiratory” acid-base disturbances increases with 637
Adding or removing an acid or base—at a constant —produces a “metabolic” acid-base disturbance 638
During metabolic disturbances, makes a greater contribution to total buffering when pH and are high and when is low 638
A metabolic change can compensate for a respiratory disturbance 641
A respiratory change can compensate for a metabolic disturbance 642
Position on a Davenport diagram defines the nature of an acid-base disturbance 643
pH Regulation of Intracellular Fluid 644
Ion transporters at the plasma membrane closely regulate the pH inside of cells 644
Indirect interactions between K+ and H+ make it appear as if cells have a K-H exchanger 645
Changes in intracellular pH are often a sign of changes in extracellular pH, and vice versa 645
References 646
References 646.e1
Books and Reviews 646.e1
Journal Articles 646.e1
29 Transport of Oxygen and Carbon Dioxide in the Blood 647
Carriage of O2 647
The amount of O2 dissolved in blood is far too small to meet the metabolic demands of the body 647
Hemoglobin consists of two α and two β subunits, each of which has an iron-containing “heme” and a polypeptide “globin” 647
The Hb-O2 dissociation curve has a sigmoidal shape because of cooperativity among the four subunits of the Hb molecule 649
Increases in temperature, [CO2], and [H+], all of which are characteristic of metabolically active tissues, cause Hb to dump O2 652
Temperature 652
Acid 652
Carbon Dioxide 653
2,3-Diphosphoglycerate reduces the affinity of adult, but not of fetal, Hb 654
Carriage of CO2 655
Blood carries “total CO2” mainly as 655
CO2 transport depends critically on carbonic anhydrase, the Cl-HCO3 exchanger, and Hb 655
The high in the lungs causes the blood to dump CO2 657
The O2-CO2 diagram describes the interaction of and in the blood 658
References 659
References 659.e1
Books and Reviews 659.e1
Journal Articles 659.e1
30 Gas Exchange in the Lungs 660
Diffusion of Gases 660
Gas flow across a barrier is proportional to diffusing capacity and concentration gradient (Fick’s law) 660
The total flux of a gas between alveolar air and blood is the summation of multiple diffusion events along each pulmonary capillary during the respiratory cycle 661
The flow of O2, CO, and CO2 between alveolar air and blood depends on the interaction of these gases with red blood cells 663
Diffusion and Perfusion Limitations on Gas Transport 664
The diffusing capacity normally limits the uptake of CO from alveolar air to blood 664
Perfusion normally limits the uptake of N2O from alveolar air to blood 666
In principle, CO transport could become perfusion limited and N2O transport could become diffusion limited under special conditions 668
The uptake of CO provides an estimate of DL 668
For both O2 and CO2, transport is normally perfusion limited 671
Uptake of O2 671
Escape of CO2 673
Pathological changes that reduce DL do not necessarily produce hypoxia 673
References 674
References 674.e1
Books and Reviews 674.e1
Journal Articles 674.e1
31 Ventilation and Perfusion of the Lungs 675
Ventilation 675
About 30% of total ventilation in a respiratory cycle is wasted ventilating anatomical dead space (i.e., conducting airways) 675
The Fowler single-breath N2-washout technique estimates anatomical dead space 676
The Bohr expired-[CO2] approach estimates physiological dead space 677
Alveolar ventilation is the ratio of CO2 production rate to CO2 mole fraction in alveolar air 679
Alveolar and arterial are inversely proportional to alveolar ventilation 679
Alveolar and arterial rise with increased alveolar ventilation 681
Because of the action of gravity on the lung, regional ventilation in an upright subject is normally greater at the base than the apex 681
Restrictive and obstructive pulmonary diseases can exacerbate the nonuniformity of ventilation 682
Restrictive Pulmonary Disease 683
Obstructive Pulmonary Disease 683
Perfusion of the Lung 683
The pulmonary circulation has low pressure and resistance but high compliance 683
Overall pulmonary vascular resistance is minimal at FRC 684
Alveolar Vessels 684
Extra-Alveolar Vessels 685
Increases in pulmonary arterial pressure reduce pulmonary vascular resistance by recruiting and distending pulmonary capillaries 685
Recruitment 686
Distention 687
Hypoxia is a strong vasoconstrictor, opposite to its effect in the systemic circulation 687
Oxygen 687
Carbon Dioxide and Low pH 687
Autonomic Nervous System 687
Hormones and Other Humoral Agents 687
Because of gravity, regional perfusion in an upright subject is far greater near the base than the apex of the lung 687
Zone 1: Pa > PPA > PPV 689
Zone 2: PPA > Pa > PPV 689
Zone 3: PPA > PPV > Pa 689
Zone 4: PPA > PPV > Pa 689
Matching Ventilation and Perfusion 689
The greater the ventilation-perfusion ratio, the higher the and the lower the in the alveolar air 689
Because of the action of gravity, the regional ratio in an upright subject is greater at the apex of the lung than at the base 690
The ventilation of unperfused alveoli (local = ∞) triggers compensatory bronchoconstriction and a fall in surfactant production 691
Alveolar Dead-Space Ventilation 691
Redirection of Blood Flow 692
Regulation of Local Ventilation 692
The perfusion of unventilated alveoli (local = 0) triggers a compensatory hypoxic vasoconstriction 692
Shunt 692
Redirection of Airflow 693
Asthma 693
Normal Anatomical Shunts 693
Pathological Shunts 693
Regulation of Local Perfusion 693
Even if whole-lung and are normal, exaggerated local mismatches produce hypoxia and respiratory acidosis 693
Normal Lungs 693
Alveolar Dead-Space Ventilation Affecting One Lung 693
Shunt Affecting One Lung 696
Mixed Mismatches 699
References 699
References 699.e1
Books and Reviews 699.e1
Journal Articles 699.e1
32 Control of Ventilation 700
Overview of the Respiratory Control System 700
Automatic centers in the brainstem activate the respiratory muscles rhythmically and subconsciously 700
Peripheral and central chemoreceptors—which sense , , and pH—drive the CPG 700
Other receptors as well as higher brain centers also modulate ventilation 702
Neurons That Control Ventilation 702
The neurons that generate the respiratory rhythm are located in the medulla 702
The pons modulates—but is not essential for—respiratory output 702
The dorsal and ventral respiratory groups contain many neurons that fire in phase with respiratory motor output 703
The dorsal respiratory group processes sensory input and contains primarily inspiratory neurons 705
The ventral respiratory group is primarily motor and contains both inspiratory and expiratory neurons 706
Generation of the Respiratory Rhythm 706
Different RRNs fire at different times during inspiration and expiration 706
The firing patterns of RRNs depend on the ion channels in their membranes and the synaptic inputs they receive 706
Intrinsic Membrane Properties 707
Synaptic Input 707
Pacemaker properties and synaptic interactions may both contribute to the generation of the respiratory rhythm 707
Pacemaker Activity 707
Synaptic Interactions 707
The respiratory CPG for eupnea could reside in a single site or in multiple sites, or could emerge from a complex network 708
Restricted-Site Model 708
Distributed Oscillator Models 708
Emergent Property Model 709
Chemical Control of Ventilation 709
Peripheral Chemoreceptors 710
Peripheral chemoreceptors (carotid and aortic bodies) respond to hypoxia, hypercapnia, and acidosis 710
Sensitivity to Decreased Arterial 710
Sensitivity to Increased Arterial 710
Sensitivity to Decreased Arterial pH 710
The glomus cell is the chemosensor in the carotid and aortic bodies 710
Hypoxia, hypercapnia, and acidosis inhibit K+ channels, raise glomus cell [Ca2+]i, and release neurotransmitters 712
Hypoxia N32-17 712
Hypercapnia 712
Extracellular Acidosis 713
Central Chemoreceptors 713
The blood-brain barrier separates the central chemoreceptors in the medulla from arterial blood 713
Central chemoreceptors are located in the ventrolateral medulla and other brainstem regions 713
Some neurons of the medullary raphé and VLM are unusually pH sensitive 714
Integrated Responses to Hypoxia, Hypercapnia, and Acidosis 716
Hypoxia accentuates the acute response to respiratory acidosis 716
Respiratory Acidosis 716
Metabolic Acidosis 716
Respiratory acidosis accentuates the acute response to hypoxia 716
Modulation of Ventilatory Control 717
Stretch and chemical/irritant receptors in the airways and lung parenchyma provide feedback about lung volume and the presence of irritants 717
Slowly Adapting Pulmonary Stretch Receptors 717
Rapidly Adapting Pulmonary Stretch (Irritant) Receptors 717
C-Fiber Receptors 717
Higher brain centers coordinate ventilation with other behaviors and can override the brainstem’s control of breathing 718
Coordination with Voluntary Behaviors That Use Respiratory Muscles 718
Coordination with Complex Nonventilatory Behaviors 720
Modification by Affective States 720
Balancing Conflicting Demands of Gas Exchange and Other Behaviors 720
References 720
References 720.e1
Books and Reviews 720.e1
Journal Articles 720.e1
VI The Urinary System 721
33 Organization of the Urinary System 722
Functional Anatomy of the Kidney 722
The kidneys are paired, retroperitoneal organs with vascular and epithelial elements 722
The kidneys have a very high blood flow and glomerular capillaries flanked by afferent and efferent arterioles 722
The functional unit of the kidney is the nephron 723
The renal corpuscle has three components: vascular elements, the mesangium, and Bowman’s capsule and space 724
The tubule components of the nephron include the proximal tubule, loop of Henle, distal tubule, and collecting duct 727
The tightness of tubule epithelia increases from the proximal to the medullary collecting tubule 729
Main Elements of Renal Function 729
The nephron forms an ultrafiltrate of the blood plasma and then selectively reabsorbs the tubule fluid or secretes solutes into it 729
The JGA is a region where each thick ascending limb contacts its glomerulus 730
Sympathetic nerve fibers to the kidney regulate renal blood flow, glomerular filtration, and tubule reabsorption 730
The kidneys, as endocrine organs, produce renin, 1,25-dihydroxyvitamin D, erythropoietin, prostaglandins, and bradykinin 730
Measuring Renal Clearance and Transport 730
The clearance of a solute is the virtual volume of plasma that would be totally cleared of a solute in a given time 731
A solute’s urinary excretion is the algebraic sum of its filtered load, reabsorption by tubules, and secretion by tubules 732
Microscopic techniques make it possible to measure single-nephron rates of filtration, absorption, and secretion 733
Single-Nephron GFR 733
Handling of Water by Tubule Segments in a Single Nephron 733
Handling of Solutes by Tubule Segments in a Single Nephron 734
The Ureters and Bladder 735
The ureters propel urine from the renal pelvis to the bladder by peristaltic waves conducted along a syncytium of smooth-muscle cells 735
Sympathetic, parasympathetic, and somatic fibers innervate the urinary bladder and its sphincters 736
Bladder filling activates stretch receptors, initiating the micturition reflex, a spinal reflex under control of higher central nervous system centers 738
References 738
References 738.e1
Books and Reviews 738.e1
Journal Articles 738.e1
34 Glomerular Filtration and Renal Blood Flow 739
Glomerular Filtration 739
A high glomerular filtration rate is essential for maintaining stable and optimal extracellular levels of solutes and water 739
The clearance of inulin is a measure of GFR 739
The clearance of creatinine is a useful clinical index of GFR 741
Molecular size and electrical charge determine the filterability of solutes across the glomerular filtration barrier 741
Hydrostatic pressure in glomerular capillaries favors glomerular ultrafiltration, whereas oncotic pressure in capillaries and hydrostatic pressure in Bowman’s space oppose it 743
Renal Blood Flow 745
Increased glomerular plasma flow leads to an increase in GFR 745
Afferent and efferent arteriolar resistances control both glomerular plasma flow and GFR 746
Peritubular capillaries provide tubules with nutrients and retrieve reabsorbed fluid 747
Blood flow in the renal cortex exceeds that in the renal medulla 749
The clearance of para-aminohippurate is a measure of RPF 749
Control of Renal Blood Flow and Glomerular Filtration 750
Autoregulation keeps RBF and GFR relatively constant 750
Myogenic Response 750
Tubuloglomerular Feedback 750
Volume expansion and a high-protein diet increase GFR by reducing TGF 751
Four factors that modulate RBF and GFR play key roles in regulating effective circulating volume 752
Renin-Angiotensin-Aldosterone Axis 752
Sympathetic Nerves 752
Arginine Vasopressin 752
Atrial Natriuretic Peptide 752
Other vasoactive agents modulate RBF and GFR 753
Epinephrine 753
Dopamine 753
Endothelins 753
Prostaglandins 753
Leukotrienes 753
Nitric Oxide 753
References 753
References 753.e2
Books and Reviews 753.e2
Journal Articles 753.e2
35 Transport of Sodium and Chloride 754
Na+ and Cl− Transport by Different Segments of The Nephron 754
Na+ and Cl− reabsorption decreases from proximal tubules to Henle’s loops to classic distal tubules to collecting tubules and ducts 754
The tubule reabsorbs Na+ via both the transcellular and the paracellular pathways 754
Transcellular Na+ Reabsorption 754
Paracellular Na+ Reabsorption 755
Na+ and Cl−, and Water Transport at the Cellular and Molecular Level 756
Na+ reabsorption involves apical transporters or ENaCs and a basolateral Na-K pump 756
Proximal Tubule 756
Thin Limbs of Henle’s Loop 757
Thick Ascending Limb 757
Distal Convoluted Tubule 758
Initial and Cortical Collecting Tubules 758
Medullary Collecting Duct 759
Cl− reabsorption involves both paracellular and transcellular pathways 759
Proximal Tubule 759
Thick Ascending Limb 759
Distal Convoluted Tubule 759
Collecting Ducts 760
Water reabsorption is passive and secondary to solute transport 761
Proximal Tubule 761
Loop of Henle and Distal Nephron 762
The kidney’s high O2 consumption reflects a high level of active Na+ transport 762
Regulation of Na+ and Cl− Transport 763
Glomerulotubular balance stabilizes fractional Na+ reabsorption by the proximal tubule in the face of changes in the filtered Na+ load 763
The proximal tubule achieves GT balance by both peritubular and luminal mechanisms 763
Peritubular Factors in the Proximal Tubule 763
Luminal Factors in the Proximal Tubule 765
ECF volume contraction or expansion upsets GT balance 765
The distal nephron also increases Na+ reabsorption in response to an increased Na+ load 765
Four parallel pathways that regulate effective circulating volume all modulate Na+ reabsorption 765
Renin-Angiotensin-Aldosterone Axis 765
Sympathetic Division of the Autonomic Nervous System 766
Arginine Vasopressin (Antidiuretic Hormone) 768
Atrial Natriuretic Peptide 768
Dopamine, elevated plasma [Ca2+], an endogenous steroid, prostaglandins, and bradykinin all decrease Na+ reabsorption 768
Dopamine 768
Elevated Plasma [Ca2+] 768
Endogenous Na-K Pump Inhibitor 768
Prostaglandins 769
Bradykinin 769
References 769
References 769.e1
Books and Reviews 769.e1
Journal Articles 769.e1
36 Transport of Urea, Glucose, Phosphate, Calcium, Magnesium, and Organic Solutes 770
Urea 770
The kidney filters, reabsorbs, and secretes urea 770
Urea excretion rises with increasing urinary flow 772
Glucose 772
The proximal tubule reabsorbs glucose via apical, electrogenic Na/glucose cotransport and basolateral facilitated diffusion 772
Glucose excretion in the urine occurs only when the plasma concentration exceeds a threshold 772
Other Organic Solutes 773
The proximal tubule reabsorbs amino acids using a wide variety of apical and basolateral transporters 773
An H+-driven cotransporter takes up oligopeptides across the apical membrane, whereas endocytosis takes up proteins and other large organic molecules 776
Oligopeptides 776
Proteins 778
Two separate apical Na+-driven cotransporters reabsorb monocarboxylates and dicarboxylates/tricarboxylates 779
The proximal tubule secretes PAH and a variety of other organic anions 779
PAH secretion is an example of a Tm-limited mechanism 781
The proximal tubule both reabsorbs and secretes urate 781
Reabsorption 783
Secretion 783
The late proximal tubule secretes several organic cations 783
Nonionic diffusion of neutral weak acids and bases across tubules explains why their excretion is pH dependent 784
Phosphate 785
The proximal tubule reabsorbs phosphate via apical Na/phosphate cotransporters 785
Phosphate excretion in the urine already occurs at physiological plasma concentrations 786
PTH inhibits apical Na/phosphate uptake, promoting phosphate excretion 786
Fibroblast growth factor 23 and other phosphatonins also inhibit apical Na/phosphate uptake, promoting phosphate excretion 787
Calcium 787
Binding to plasma proteins and formation of Ca2+-anion complexes influence the filtration and reabsorption of Ca2 787
The proximal tubule reabsorbs two thirds of filtered Ca2+, with more distal segments reabsorbing nearly all of the remainder 787
Proximal Tubule 787
Thick Ascending Limb 787
Distal Convoluted Tubule 787
Transcellular Ca2+ movement is a two-step process, involving passive Ca2+ entry through apical channels and basolateral extrusion by electrogenic Na/Ca exchange and a Ca pump 788
PTH and vitamin D stimulate—whereas high plasma Ca2+ inhibits—Ca2+ reabsorption 789
Parathyroid Hormone 789
Vitamin D 789
Plasma Ca2+ Levels 789
Diuretics 789
Magnesium 789
Most Mg2+ reabsorption takes place along the TAL 789
Mg2+ reabsorption increases with depletion of Mg2+ or Ca2+, or with elevated PTH levels 791
Mg2+ Depletion 791
Hypermagnesemia and Hypercalcemia 791
Hormones 791
Diuretics 791
References 791
References 791.e2
Books and Reviews 791.e2
Journal Articles 791.e2
37 Transport of Potassium 792
Potassium Balance and the Overall Renal Handling of Potassium 792
Changes in K+ concentrations can have major effects on cell and organ function 792
K+ homeostasis involves external K+ balance between environment and body, and internal K+ balance between intracellular and extracellular compartments 792
External K+ Balance 792
Internal K+ Balance 792
Ingested K+ moves transiently into cells for storage before excretion by the kidney 792
The kidney excretes K+ by a combination of filtration, reabsorption, and secretion 795
Potassium Transport by Different Segments of the Nephron 795
The proximal tubule reabsorbs most of the filtered K+, whereas the distal nephron reabsorbs or secretes K+, depending on K+ intake 795
Low Dietary K 795
Normal or High Dietary K 796
Medullary trapping of K+ helps to maximize K+ excretion when K+ intake is high 796
Potassium Transport at the Cellular and Molecular Levels 797
Passive K+ reabsorption along the proximal tubule follows Na+ and fluid movements 797
K+ reabsorption along the TAL occurs predominantly via a transcellular route that exploits secondary active Na/K/Cl cotransport 798
K+ secretion by principal and intercalated cells of the ICT and CCT involves active K+ uptake across the basolateral membrane 799
K+ reabsorption by intercalated cells involves apical uptake via an H-K pump 799
K+ reabsorption along the MCD is both passive and active 799
Regulation of Renal Potassium Excretion 799
Increased luminal flow increases K+ secretion 799
An increased lumen-negative transepithelial potential increases K+ secretion 800
Low luminal [Cl−] enhances K+ secretion 800
Aldosterone increases K+ secretion 800
Mineralocorticoids 800
Glucocorticoids 801
High K+ intake promotes renal K+ secretion 801
Dietary K+ Loading 801
Dietary K+ Deprivation 803
Acidosis decreases K+ secretion 803
Epinephrine reduces and AVP enhances K+ excretion 803
Opposing factors stabilize K+ secretion 803
Attenuating Effects 804
Additive Effects 804
References 805
References 805.e2
Books and Reviews 805.e2
Journal Articles 805.e2
38 Urine Concentration and Dilution 806
Water Balance and the Overall Renal Handling of Water 806
The kidney can generate a urine as dilute as 40 mOsm (one seventh of plasma osmolality) or as concentrated as 1200 mOsm (four times plasma osmolality) 806
Free-water clearance () is positive if the kidney produces urine that is less concentrated than plasma and negative if the kidney produces urine that is more concentrated than plasma 806
Isosmotic Urine 807
Dilute Urine 807
Concentrated Urine 807
Water Transport by Different Segments of the Nephron 807
The kidney concentrates urine by driving water via osmosis from the tubule lumen into a hyperosmotic interstitium 807
Tubule fluid is isosmotic in the proximal tubule, becomes dilute in the loop of Henle, and then either remains dilute or becomes concentrated by the end of the collecting duct 808
Generation of a Hyperosmotic Medulla and Urine 809
The renal medulla is hyperosmotic to blood plasma during both antidiuresis (low urine flow) and water diuresis 809
NaCl transport generates only a ~200-mOsm gradient across any portion of the ascending limb, but countercurrent exchange can multiply this single effect to produce a 900-mOsm gradient between cortex and papilla 809
The single effect is the result of passive NaCl reabsorption in the thin ascending limb and active NaCl reabsorption in the TAL 811
The IMCD reabsorbs urea, producing high levels of urea in the interstitium of the inner medulla 811
Urea Handling 811
Urea Recycling 813
The vasa recta’s countercurrent exchange and relatively low blood flow minimize washout of medullary hyperosmolality 813
The MCD produces a concentrated urine by osmosis, driven by the osmotic gradient between the medullary interstitium and the lumen 816
Regulation by Arginine Vasopressin 817
AVP increases water permeability in all nephron segments beyond the DCT 817
AVP, via cAMP, causes vesicles containing AQP2 to fuse with apical membranes of principal cells of collecting tubules and ducts 818
AVP increases NaCl reabsorption in the outer medulla and urea reabsorption in the IMCD, enhancing urinary concentrating ability 818
References 820
References 820.e2
Books and Reviews 820.e2
Journal Articles 820.e2
39 Transport of Acids and Bases 821
Acid-Base Balance and the Overall Renal Handling of Acid 821
Whereas the lungs excrete the large amount of CO2 formed by metabolism, the kidneys are crucial for excreting nonvolatile acids 821
To maintain acid-base balance, the kidney must not only reabsorb virtually all filtered but also secrete generated nonvolatile acids 821
Secreted H+ titrates to CO2 ( reabsorption) and also titrates filtered buffers and endogenously produced NH3 823
Titration of Filtered (“ Reabsorption”) 823
Titration of Filtered Buffers (Titratable-Acid Formation) 824
Titration of Filtered and Secreted NH3 (Ammonium Excretion) 825
Acid-Base Transport by Different Segments of the Nephron 825
The nephron reclaims virtually all the filtered in the proximal tubule (~80%), thick ascending limb (~10%), and distal nephron (~10%) 825
The nephron generates new , mostly in the proximal tubule 825
Formation of Titratable Acid 825
Excretion 826
Acid-Base Transport at the Cellular and Molecular Levels 827
H+ moves across the apical membrane from tubule cell to lumen by Na-H exchange, electrogenic H pumping, and K-H pumping 827
Na-H Exchanger 827
Electrogenic H Pump 827
H-K Exchange Pump 827
CAs in the lumen and cytosol stimulate H+ secretion by accelerating the interconversion of CO2 and 828
Apical CA (CA IV) 828
Cytoplasmic CA (CA II) 828
Basolateral CA (CA IV and CA XII) 828
Inhibition of CA 829
efflux across the basolateral membrane takes place by electrogenic Na/HCO3 cotransport and Cl-HCO3 exchange 829
Electrogenic Na/HCO3 Cotransport 829
Cl-HCO3 Exchange 829
is synthesized by proximal tubules, partly reabsorbed in the loop of Henle, and secreted passively into papillary collecting ducts 829
Regulation of Renal Acid Secretion 832
Respiratory acidosis stimulates renal H+ secretion 832
Metabolic acidosis stimulates both proximal H+ secretion and NH3 production 833
Metabolic alkalosis reduces proximal H+ secretion and, in the CCT, may even provoke secretion 833
A rise in GFR increases delivery to the tubules, enhancing reabsorption (glomerulotubular balance for ) 834
Extracellular volume contraction—via ANG II, aldosterone, and sympathetic activity—stimulates renal H+ secretion 834
Hypokalemia increases renal H+ secretion 834
Both glucocorticoids and mineralocorticoids stimulate acid secretion 835
Diuretics can change H+ secretion, depending on how they affect transepithelial voltage, ECF volume, and plasma [K+] 835
References 835
References 835.e2
Books and Reviews 835.e2
Journal Articles 835.e2
40 Integration of Salt and Water Balance 836
Sodium Balance 836
Water Balance 836
Control of Extracellular Fluid Volume 836
In the steady state, Na+ intake via the gastrointestinal tract equals Na+ output from renal and extrarenal pathways 836
The kidneys increase Na+ excretion in response to an increase in ECF volume, not to an increase in extracellular Na+ concentration 837
It is not the ECF volume as a whole, but the effective circulating volume, that regulates Na+ excretion 838
Decreases in effective circulating volume trigger four parallel effector pathways to decrease renal Na+ excretion 838
Increased activity of the renin-angiotensin-aldosterone axis is the first of four parallel pathways that correct a low effective circulating volume 841
Increased sympathetic nerve activity, increased AVP, and decreased ANP are the other three parallel pathways that correct a low effective circulating volume 842
Renal Sympathetic Nerve Activity 842
Arginine Vasopressin (Antidiuretic Hormone) 843
Atrial Natriuretic Peptide 843
High arterial pressure raises Na+ excretion by hemodynamic mechanisms, independent of changes in effective circulating volume 843
Large and Acute Decrease in Arterial Blood Pressure 843
Large Increase in Arterial Pressure 843
Control of Water Content (Extracellular Osmolality) 844
Increased plasma osmolality stimulates hypothalamic osmoreceptors that trigger the release of AVP, inhibiting water excretion 844
Hypothalamic neurons synthesize AVP and transport it along their axons to the posterior pituitary, where they store it in nerve terminals prior to release 844
Increased osmolality stimulates a second group of osmoreceptors that trigger thirst, which promotes water intake 845
Several nonosmotic stimuli also enhance AVP secretion 846
Reduced Effective Circulating Volume 846
Volume Expansion 847
Pregnancy 847
Other Factors 848
Decreased effective circulating volume and low arterial pressure also trigger thirst 849
Defense of the effective circulating volume usually has priority over defense of osmolality 849
References 849
References 849.e2
Books and Reviews 849.e2
Journal Articles 849.e2
VII The Gastrointestinal System 851
41 Organization of the Gastrointestinal System 852
Overview of Digestive Processes 852
The gastrointestinal tract is a tube that is specialized along its length for the sequential processing of food 852
Assimilation of dietary food substances requires digestion as well as absorption 852
Digestion requires enzymes secreted in the mouth, stomach, pancreas, and small intestine 853
Ingestion of food initiates multiple endocrine, neural, and paracrine responses 853
In addition to its function in nutrition, the GI tract plays important roles in excretion, fluid and electrolyte balance, and immunity 855
Regulation of Gastrointestinal Function 855
The ENS is a “minibrain” with sensory neurons, interneurons, and motor neurons 855
ACh, peptides, and bioactive amines are the ENS neurotransmitters that regulate epithelial and motor function 856
The brain-gut axis is a bidirectional system that controls GI function via the ANS, GI hormones, and the immune system 856
Gastrointestinal Motility 858
Tonic and rhythmic contractions of smooth muscle are responsible for churning, peristalsis, and reservoir action 858
Segments of the GI tract have both longitudinal and circular arrays of muscles and are separated by sphincters that consist of specialized circular muscles 858
Location of a sphincter determines its function 859
Upper Esophageal Sphincter 859
Lower Esophageal Sphincter 859
Pyloric Sphincter 860
Ileocecal Sphincter 860
Internal and External Anal Sphincters 860
Motility of the small intestine achieves both churning and propulsive movement, and its temporal pattern differs in the fed and fasted states 860
Motility of the large intestine achieves both propulsive movement and a reservoir function 862
References 862
References 862.e2
Books and Reviews 862.e2
Journal Articles 862.e2
42 Gastric Function 863
Functional Anatomy of the Stomach 863
The mucosa is composed of surface epithelial cells and glands 863
With increasing rates of secretion of gastric juice, the H+ concentration rises and the Na+ concentration falls 863
The proximal portion of the stomach secretes acid, pepsinogens, intrinsic factor, bicarbonate, and mucus, whereas the distal part releases gastrin and somatostatin 863
Corpus 863
Antrum 865
The stomach accommodates food, mixes it with gastric secretions, grinds it, and empties the chyme into the duodenum 865
Acid Secretion 865
The parietal cell has a specialized tubulovesicular structure that increases apical membrane area when the cell is stimulated to secrete acid 865
An H-K pump is responsible for gastric acid secretion by parietal cells 865
Three secretagogues (acetylcholine, gastrin, and histamine) directly and indirectly induce acid secretion by parietal cells 866
The three acid secretagogues act through either Ca2+/diacylglycerol or cAMP 867
Antral and duodenal G cells release gastrin, whereas ECL cells in the corpus release histamine 867
Gastric D cells release somatostatin, the central inhibitor of acid secretion 868
Several enteric hormones (“enterogastrone”) and prostaglandins inhibit gastric acid secretion 870
A meal triggers three phases of acid secretion 870
Basal State 870
Cephalic Phase 871
Gastric Phase 871
Intestinal Phase 872
Pepsinogen Secretion 872
Chief cells, triggered by both cAMP and Ca2+ pathways, secrete multiple pepsinogens that initiate protein digestion 872
Agonists Acting via cAMP 873
Agonists Acting via Ca2 873
Low pH is required for both pepsinogen activation and pepsin activity 873
Protection of the Gastric Surface Epithelium and Neutralization of Acid in the Duodenum 874
Vagal stimulation and irritation stimulate gastric mucous cells to secrete mucins 874
Gastric surface cells secrete , stimulated by acetylcholine, acids, and prostaglandins 874
Mucus protects the gastric surface epithelium by trapping an -rich fluid near the apical border of these cells 874
Acid entry into the duodenum induces S cells to release secretin, triggering the pancreas and duodenum to secrete 875
Filling and Emptying of the Stomach 876
Gastric motor activity plays a role in filling, churning, and emptying 876
Filling of the stomach is facilitated by both receptive relaxation and gastric accommodation 877
The stomach churns its contents until the particles are small enough to be gradually emptied into the duodenum 877
References 878
References 878.e1
Books and Reviews 878.e1
Journal Articles 878.e1
43 Pancreatic and Salivary Glands 879
Overview of Exocrine Gland Physiology 879
The pancreas and major salivary glands are compound exocrine glands 879
Acinar cells are specialized protein-synthesizing cells 879
Duct cells are epithelial cells specialized for fluid and electrolyte transport 881
Goblet cells contribute to mucin production in exocrine glands 881
Pancreatic Acinar Cell 882
The acinar cell secretes digestive proteins in response to stimulation 882
Acetylcholine and cholecystokinin mediate the regulated secretion of proteins by pancreatic acinar cells 882
Ca2+ is the major second messenger for the secretion of proteins by pancreatic acinar cells 883
Ca2 883
cAMP 883
Effectors 884
In addition to proteins, the pancreatic acinar cell secretes a plasma-like fluid 884
Pancreatic Duct Cell 885
The pancreatic duct cell secretes isotonic NaHCO3 885
Secretin (via cAMP) and ACh (via Ca2+) stimulate secretion by pancreatic ducts 886
Apical membrane chloride channels are important sites of neurohumoral regulation 887
Pancreatic duct cells may also secrete glycoproteins 887
Composition, Function, and Control of Pancreatic Secretion 887
Pancreatic juice is a protein-rich, alkaline secretion 887
In the fasting state, levels of secreted pancreatic enzymes oscillate at low levels 888
CCK from duodenal I cells stimulates acinar enzyme secretion, and secretin from S cells stimulates and fluid secretion by ducts 889
A meal triggers cephalic, gastric, and intestinal phases of pancreatic secretion 890
Cephalic Phase 890
Gastric Phase 890
Intestinal Phase 890
The pancreas has large reserves of digestive enzymes for carbohydrates and proteins, but not for lipids 892
Fat in the distal part of the small intestine inhibits pancreatic secretion 892
Several mechanisms protect the pancreas from autodigestion 892
Salivary Acinar Cell 893
Different salivary acinar cells secrete different proteins 893
Cholinergic and adrenergic neural pathways are the most important physiological activators of regulated secretion by salivary acinar cells 894
Both cAMP and Ca2+ mediate salivary acinar secretion 894
Salivary Duct Cell 894
Salivary duct cells produce a hypotonic fluid that is poor in NaCl and rich in KHCO3 894
Parasympathetic stimulation decreases Na+ absorption, whereas aldosterone increases Na+ absorption by duct cells 895
Salivary duct cells also secrete and take up proteins 895
Composition, Function, and Control of Salivary Secretion 896
Depending on protein composition, salivary secretions can be serous, seromucous, or mucous 896
At low flow rates, the saliva is hypotonic and rich in K+, whereas at higher flow rates, its composition approaches that of plasma 896
Parasympathetic stimulation increases salivary secretion 897
Parasympathetic Control 897
Sympathetic Control 897
References 898
References 898.e1
Books and Reviews 898.e1
Journal Articles 898.e1
44 Intestinal Fluid and Electrolyte Movement 899
Functional Anatomy 899
Both the small and large intestine absorb and secrete fluid and electrolytes, whereas only the small intestine absorbs nutrients 899
The small intestine has a villus-crypt organization, whereas the colon has surface epithelial cells with interspersed crypts 899
The surface area of the small intestine is amplified by folds, villi, and microvilli; amplification is less marked in the colon 901
Overview of Fluid and Electrolyte Movement in the Intestines 901
The small intestine absorbs ~6.5 L/day of an ~8.5-L fluid load that is presented to it, and the colon absorbs ~1.9 L/day 901
The small intestine absorbs net amounts of water, Na+, Cl−, and K+ and secretes , whereas the colon absorbs net amounts of water, Na+, and Cl− and secretes both K+ and 901
The intestines absorb and secrete solutes by both active and passive mechanisms 902
Intestinal fluid movement is always coupled to solute movement, and sometimes solute movement is coupled to fluid movement by solvent drag 903
The resistance of the tight junctions primarily determines the transepithelial resistance of intestinal epithelia 903
Cellular Mechanisms of Na+ Absorption 903
Na/glucose and Na/amino-acid cotransport in the small intestine is a major mechanism for postprandial Na+ absorption 903
Electroneutral Na-H exchange in the duodenum and jejunum is responsible for Na+ absorption that is stimulated by luminal alkalinity 904
Parallel Na-H and Cl-HCO3 exchange in the ileum and proximal part of the colon is the primary mechanism of Na+ absorption during the interdigestive period 905
Epithelial Na+ channels are the primary mechanism of “electrogenic” Na+ absorption in the distal part of the colon 905
Cellular Mechanisms of Cl− Absorption and Secretion 905
Voltage-dependent Cl− absorption represents coupling of Cl− absorption to electrogenic Na+ absorption in both the small intestine and the large intestine 906
Electroneutral Cl-HCO3 exchange results in Cl− absorption and secretion in the ileum and colon 906
Parallel Na-H and Cl-HCO3 exchange in the ileum and the proximal part of the colon mediates Cl− absorption during the interdigestive period 907
Electrogenic Cl− secretion occurs in crypts of both the small and the large intestine 907
Cellular Mechanisms of K+ Absorption and Secretion 908
Overall net transepithelial K+ movement is absorptive in the small intestine and secretory in the colon 908
K+ absorption in the small intestine probably occurs via solvent drag 908
Passive K+ secretion is the primary mechanism for net colonic secretion 908
Active K+ secretion is also present throughout the large intestine and is induced both by aldosterone and by cAMP 909
Aldosterone 909
cAMP and Ca2 909
Active K+ absorption takes place only in the distal portion of the colon and is energized by an apical H-K pump 910
Regulation of Intestinal Ion Transport 910
Chemical mediators from the enteric nervous system, endocrine cells, and immune cells in the lamina propria may be either secretagogues or absorptagogues 910
Secretagogues can be classified by their type and by the intracellular second-messenger system that they stimulate 910
Mineralocorticoids, glucocorticoids, and somatostatin are absorptagogues 912
References 913
References 913.e1
Books and Reviews 913.e1
Journal Articles 913.e1
45 Nutrient Digestion and Absorption 914
Carbohydrate Digestion 914
Carbohydrates, providing ~45% of total energy needs of Western diets, require hydrolysis to monosaccharides before absorption 914
Luminal digestion begins with the action of salivary amylase and finishes with pancreatic amylase 916
“Membrane digestion” involves hydrolysis of oligosaccharides to monosaccharides by brush-border disaccharidases 916
Carbohydrate Absorption 919
SGLT1 is responsible for the Na+-coupled uptake of glucose and galactose across the apical membrane 919
The GLUT transporters mediate the facilitated diffusion of fructose at the apical membrane and of all three monosaccharides at the basolateral membrane 919
Protein Digestion 920
Proteins require hydrolysis to oligopeptides or amino acids before absorption in the small intestine 920
Luminal digestion of protein involves both gastric and pancreatic proteases, and yields amino acids and oligopeptides 921
Brush-border peptidases fully digest some oligopeptides to amino acids, whereas cytosolic peptidases digest oligopeptides that directly enter the enterocyte 922
Protein, Peptide, and Amino-Acid Absorption 922
Absorption of whole protein by apical endocytosis occurs primarily during the neonatal period 922
The apical absorption of dipeptides, tripeptides, and tetrapeptides occurs via an H+-driven cotransporter 922
Amino acids enter enterocytes via one or more group-specific apical transporters 923
At the basolateral membrane, amino acids exit enterocytes via Na+-independent transporters and enter via Na+-dependent transporters 923
Lipid Digestion 925
Natural lipids of biological origin are sparingly soluble in water 925
Dietary lipids are predominantly TAGs 925
Endogenous lipids are phospholipids and cholesterol from bile and membrane lipids from desquamated intestinal epithelial cells 927
The mechanical disruption of dietary lipids in the mouth and stomach produces an emulsion of lipid particles 927
Lingual and gastric (acid) lipase initiate lipid digestion 927
Pancreatic (alkaline) lipase, colipase, milk lipase, and other esterases—aided by bile salts—complete lipid hydrolysis in the duodenum and jejunum 928
Lipid Absorption 929
Products of lipolysis enter the bulk water phase of the intestinal lumen as vesicles, mixed micelles, and monomers 929
Lipids diffuse as mixed micelles and monomers through unstirred layers before crossing the jejunal enterocyte brush border 930
The enterocyte re-esterifies lipid components and assembles them into chylomicrons 930
The enterocyte secretes chylomicrons into the lymphatics during feeding and secretes VLDLs during fasting 932
Digestion and Absorption of Vitamins and Minerals 933
Intestinal absorption of fat-soluble vitamins follows the pathways of lipid absorption and transport 933
Dietary folate (PteGlu7) must be deconjugated by a brush-border enzyme before absorption by an anion exchanger at the apical membrane 933
Vitamin B12 (cobalamin) binds to haptocorrin in the stomach and then to intrinsic factor in the small intestine before endocytosis by enterocytes in the ileum 935
Ca2+ absorption, regulated primarily by vitamin D, occurs by active transport in the duodenum and by diffusion throughout the small intestine 938
Mg2+ absorption occurs by an active process in the ileum 939
Heme and nonheme iron are absorbed in the duodenum by distinct cellular mechanisms 939
Nonheme Iron 939
Heme Iron 941
Nutritional Requirements 941
No absolute daily requirement for carbohydrate or fat intake exists 941
The daily protein requirement for adult humans is typically 0.8 g/kg body weight but is higher in pregnant women, postsurgical patients, and athletes 941
Minerals and vitamins are not energy sources but are necessary for certain enzymatic reactions, for protein complexes, or as precursors for biomolecules 942
Minerals 942
Vitamins 942
Excessive intake of vitamins and minerals has mixed effects on bodily function 943
References 943
References 943.e1
Books and Reviews 943.e1
Journal Articles 943.e1
46 Hepatobiliary Function 944
Overview of Liver Physiology 944
The liver biotransforms and degrades substances taken up from blood and either returns them to the circulation or excretes them into bile 944
The liver stores carbohydrates, lipids, vitamins, and minerals; it synthesizes carbohydrates, protein, and intermediary metabolites 944
Functional Anatomy of the Liver and Biliary Tree 944
Hepatocytes are secretory epithelial cells separating the lumen of bile canaliculi from the fenestrated endothelium of sinusoids 944
The liver contains endothelial cells, macrophages (Kupffer cells), and stellate cells (Ito cells) within the sinusoidal spaces 946
The liver has a dual blood supply, but a single venous drainage system 946
Hepatocytes can be thought of as being arranged as classic hepatic lobules, portal lobules, or acinar units 946
Periportal hepatocytes specialize in oxidative metabolism, whereas pericentral hepatocytes detoxify drugs 946
Bile drains from canaliculi into small terminal ductules, then into larger ducts, and eventually, via a single common duct, into the duodenum 948
Uptake, Processing, and Secretion of Compounds by Hepatocytes 949
An Na-K pump at the basolateral membranes of hepatocytes provides the energy for transporting a wide variety of solutes via channels and transporters 951
Hepatocytes take up bile acids, other organic anions, and organic cations across their basolateral (sinusoidal) membranes 951
Bile Acids and Salts 951
Organic Anions 951
Bilirubin 951
Organic Cations 953
Neutral Organic Compounds 954
Inside the hepatocyte, the basolateral-to-apical movement of many compounds occurs by protein-bound or vesicular routes 954
Bile Salts 954
Bilirubin 954
In phase I of the biotransformation of organic anions and other compounds, hepatocytes use mainly cytochrome P-450 enzymes 954
In phase II of biotransformation, conjugation of phase I products makes them more water soluble for secretion into blood or bile 955
In phase III of biotransformation, hepatocytes excrete products of phase I and II into bile or sinusoidal blood 956
The interactions of xenobiotics with nuclear receptors control phase I, II, and III 956
Hepatocytes secrete bile acids, organic anions, organic cations, and lipids across their apical (canalicular) membranes 957
Bile Salts 957
Organic Anions 957
Organic Cations 957
Biliary Lipids 957
Hepatocytes take up proteins across their basolateral membranes by receptor-mediated endocytosis and fluid-phase endocytosis 957
Bile Formation 958
The secretion of canalicular bile is active and isotonic 958
Major organic molecules in bile include bile acids, cholesterol, and phospholipids 958
Canalicular bile flow has a constant component driven by the secretion of small organic molecules and a variable component driven by the secretion of bile acids 959
Bile Acid–Independent Flow in the Canaliculi 960
Bile Acid–Dependent Flow in the Canaliculi 960
Secretin stimulates the cholangiocytes of ductules and ducts to secrete a watery, -rich fluid 960
The gallbladder stores bile and delivers it to the duodenum during a meal 961
The relative tones of the gallbladder and sphincter of Oddi determine whether bile flows from the common hepatic duct into the gallbladder or into the duodenum 961
Enterohepatic Circulation of Bile Acids 962
The enterohepatic circulation of bile acids is a loop consisting of secretion by the liver, reabsorption by the intestine, and return to the liver in portal blood for repeat secretion into bile 962
Efficient intestinal conservation of bile acids depends on active apical absorption in the terminal ileum and passive absorption throughout the intestinal tract 962
The Liver as a Metabolic Organ 964
The liver can serve as either a source or a sink for glucose 964
The liver synthesizes a variety of important plasma proteins (e.g., albumin, coagulation factors, and carriage proteins) and metabolizes dietary amino acids 965
Protein Synthesis 965
Amino-Acid Uptake 965
Amino-Acid Metabolism 965
The liver obtains dietary triacylglycerols and cholesterol by taking up remnant chylomicrons via receptor-mediated endocytosis 966
Cholesterol, synthesized primarily in the liver, is an important component of cell membranes and serves as a precursor for bile acids and steroid hormones 968
Synthesis of Cholesterol 968
The liver is the central organ for cholesterol homeostasis and for the synthesis and degradation of LDL 969
The liver is the prime site for metabolism and storage of the fat-soluble vitamins A, D, E, and K 970
Vitamin A 970
Vitamin D 970
Vitamin E 970
Vitamin K 970
The liver stores copper and iron 970
Copper 970
Iron 971
References 971
References 971.e1
Books and Reviews 971.e1
Journal Articles 971.e1
VIII The Endocrine System 973
47 Organization of Endocrine Control 974
Principles of Endocrine Function 974
Chemical signaling can occur through endocrine, paracrine, or autocrine pathways 974
Endocrine Glands 974
Paracrine Factors 974
Hormones may be peptides, metabolites of single amino acids, or metabolites of cholesterol 975
Hormones can circulate either free or bound to carrier proteins 976
Immunoassays allow measurement of circulating hormones 976
Hormones can have complementary and antagonistic actions 976
Endocrine regulation occurs through feedback control 977
Endocrine regulation can involve hierarchic levels of control 978
The anterior pituitary regulates reproduction, growth, energy metabolism, and stress responses 978
The posterior pituitary regulates water balance and uterine contraction 979
Peptide Hormones 981
Specialized endocrine cells synthesize, store, and secrete peptide hormones 981
Peptide hormones bind to cell-surface receptors and activate a variety of signal-transduction systems 981
G Proteins Coupled to Adenylyl Cyclase 982
G Proteins Coupled to Phospholipase C 982
G Proteins Coupled to Phospholipase A2 984
Guanylyl Cyclase 984
Receptor Tyrosine Kinases 984
Tyrosine Kinase–Associated Receptors 984
Amine Hormones 984
Amine hormones are made from tyrosine and tryptophan 984
Amine hormones act via surface receptors 984
Steroid and Thyroid Hormones 985
Cholesterol is the precursor for the steroid hormones: cortisol, aldosterone, estradiol, progesterone, and testosterone 985
Steroid hormones bind to intracellular receptors that regulate gene transcription 986
Thyroid hormones bind to intracellular receptors that regulate metabolic rate 988
Steroid and thyroid hormones can also have nongenomic actions 989
References 989
References 989.e1
Books and Reviews 989.e1
Journal Articles 989.e1
48 Endocrine Regulation of Growth and Body Mass 990
Growth Hormone 990
GH, secreted by somatotrophs in the anterior pituitary, is the principal endocrine regulator of growth 990
GH is in a family of hormones with overlapping activity 991
Somatotrophs secrete GH in pulses 991
GH secretion is under hierarchical control by GH–releasing hormone and somatostatin 992
GH-Releasing Hormone 992
GHRH Receptor 992
Ghrelin 992
Ghrelin Receptor 993
Somatostatin 993
SS Receptor 994
Both GH and IGF-1 negatively feed back on GH secretion by somatotrophs 994
GH has short-term anti-insulin metabolic effects as well as long-term growth-promoting effects mediated by IGF-1 994
GH Receptor 994
Short-Term Effects of GH 994
Long-Term Effects of GH via IGF-1 994
Growth-Promoting Hormones 996
IGF-1 is the principal mediator of the growth-promoting action of GH 996
IGF-2 acts similarly to IGF-1 but is less dependent on GH 996
Growth rate parallels plasma levels of IGF-1 except early and late in life 998
Thyroid hormones, steroids, and insulin also promote growth 999
Thyroid Hormones 999
Sex Steroids 999
Glucocorticoids 999
Insulin 999
The musculoskeletal system responds to growth stimuli of the GHRH–GH–IGF-1 axis 1000
Regulation of Body Mass 1000
The balance between energy intake and expenditure determines body mass 1001
Energy expenditure comprises resting metabolic rate, activity-related energy expenditure, and diet-induced thermogenesis 1001
Hypothalamic centers control the sensations of satiety and hunger 1001
Leptin tells the brain how much fat is stored 1001
Leptin and insulin are anorexigenic (i.e., satiety) signals for the hypothalamus 1002
POMC Neurons 1002
NPY/AgRP Neurons 1002
Secondary Neurons 1003
Ghrelin is an orexigenic signal for the hypothalamus 1003
Plasma nutrient levels and enteric hormones are short-term factors that regulate feeding 1003
References 1005
References 1005.e1
Books and Reviews 1005.e1
Journal Articles 1005.e1
49 The Thyroid Gland 1006
Synthesis of Thyroid Hormones 1006
T4 and T3, made by iodination of tyrosine residues on thyroglobulin, are stored as part of thyroglobulin molecules in thyroid follicles 1006
Follicular cells take up iodinated thyroglobulin, hydrolyze it, and release T4 and T3 into the blood for binding to plasma proteins 1007
Peripheral tissues deiodinate T4 to produce T3 1009
Action of Thyroid Hormones 1010
Thyroid hormones act through nuclear receptors in target tissues 1010
Thyroid hormones can also act by nongenomic pathways 1011
Thyroid hormones increase basal metabolic rate by stimulating futile cycles of catabolism and anabolism 1011
Carbohydrate Metabolism 1012
Protein Metabolism 1012
Lipid Metabolism 1012
Na-K Pump Activity 1012
Thermogenesis 1013
Thyroid hormones are essential for normal growth and development 1013
Hypothalamic-Pituitary-Thyroid Axis 1014
TRH from the hypothalamus stimulates thyrotrophs of the anterior pituitary to secrete TSH, which stimulates T4/T3 synthesis 1014
Thyrotropin-Releasing Hormone 1014
TRH Receptor 1014
Thyrotropin 1016
TSH Receptor 1016
T3 exerts negative feedback on TSH secretion 1016
References 1017
References 1017.e2
Books and Reviews 1017.e2
Journal Articles 1017.e2
50 The Adrenal Gland 1018
The Adrenal Cortex: Cortisol 1018
Cortisol is the primary glucocorticoid hormone in humans 1018
Target Tissues 1018
Actions 1018
The adrenal zona fasciculata converts cholesterol to cortisol 1019
Cortisol binds to a cytoplasmic receptor that translocates to the nucleus and modulates transcription in multiple tissues 1022
Corticotropin-releasing hormone from the hypothalamus stimulates anterior pituitary corticotrophs to secrete ACTH, which stimulates the adrenal cortex to synthesize and secrete cortisol 1023
Corticotropin-Releasing Hormone 1023
CRH Receptor 1023
Arginine Vasopressin 1023
Adrenocorticotropic Hormone 1023
ACTH Receptor 1023
Cortisol exerts negative feedback on CRH and ACTH secretion, whereas stress acts through higher CNS centers to stimulate the axis 1025
Feedback to the Anterior Pituitary 1025
Feedback to the Hypothalamus 1025
Control by a Higher CNS Center 1025
The Adrenal Cortex: Aldosterone 1026
The mineralocorticoid aldosterone is the primary regulator of salt balance and extracellular volume 1026
The glomerulosa cells of the adrenal cortex synthesize aldosterone from cholesterol via progesterone 1026
Aldosterone stimulates Na+ reabsorption and K+ excretion by the renal tubule 1027
Angiotensin II, K+, and ACTH all stimulate aldosterone secretion 1027
Angiotensin II 1028
Potassium 1028
Adrenocorticotropic Hormone 1028
Aldosterone exerts indirect negative feedback on the renin-angiotensin axis by increasing effective circulating volume and by lowering plasma [K+] 1029
Renin-Angiotensin Axis 1029
Potassium 1029
Role of Aldosterone in Normal Physiology 1030
Role of Aldosterone in Disease 1030
The Adrenal Medulla 1030
The adrenal medulla bridges the endocrine and sympathetic nervous systems 1030
Only chromaffin cells of the adrenal medulla have the enzyme for epinephrine synthesis 1030
Catecholamines bind to α and β adrenoceptors on the cell surface and act through heterotrimeric G proteins 1033
The CNS-epinephrine axis provides integrated control of multiple functions 1033
References 1034
References 1034.e1
Books and Reviews 1034.e1
Journal Articles 1034.e1
51 The Endocrine Pancreas 1035
The islets of Langerhans are endocrine and paracrine tissue 1035
Insulin 1035
Insulin replenishes fuel reserves in muscle, liver, and adipose tissue 1036
β cells synthesize and secrete insulin 1037
The Insulin Gene 1037
Insulin Synthesis 1037
Secretion of Insulin, Proinsulin, and C Peptide 1037
Glucose is the major regulator of insulin secretion 1038
Metabolism of glucose by the β cell triggers insulin secretion 1039
Neural and humoral factors modulate insulin secretion 1041
Exercise 1041
Feeding 1041
The insulin receptor is a receptor tyrosine kinase 1041
High levels of insulin lead to downregulation of insulin receptors 1044
In liver, insulin promotes conversion of glucose to glycogen stores or to triacylglycerols 1044
Glycogen Synthesis and Glycogenolysis 1044
Glycolysis and Gluconeogenesis 1045
Lipogenesis 1047
Protein Metabolism 1047
In muscle, insulin promotes the uptake of glucose and its storage as glycogen 1047
In adipocytes, insulin promotes glucose uptake and conversion to TAGs for storage 1047
Glucagon 1050
Pancreatic α cells secrete glucagon in response to ingested protein 1050
Pancreatic α Cells 1050
Intestinal L Cells 1051
Glucagon, acting through cAMP, promotes the synthesis of glucose by the liver 1051
Glucagon promotes oxidation of fat in the liver, which can lead to ketogenesis 1051
Somatostatin 1053
Somatostatin inhibits the secretion of growth hormone, insulin, and other hormones 1053
References 1053
References 1053.e1
Books and Reviews 1053.e1
Journal Articles 1053.e1
52 The Parathyroid Glands and Vitamin D 1054
Calcium and Phosphate Balance 1054
The gut, kidneys, and bone regulate calcium balance 1054
The gut, kidneys, and bone also regulate phosphate balance 1054
Physiology of Bone 1056
Dense cortical bone and the more reticulated trabecular bone are the two major bone types 1056
The extracellular matrix forms the nidus for the nucleation of hydroxyapatite crystals 1057
Bone remodeling depends on the closely coupled activities of osteoblasts and osteoclasts 1057
Parathyroid Hormone 1058
Plasma Ca2+ regulates the synthesis and secretion of PTH 1058
PTH Synthesis and Vitamin D 1058
Processing of PTH 1059
Metabolism of PTH 1059
High plasma [Ca2+] inhibits the synthesis and release of PTH 1060
The PTH receptor couples via G proteins to either adenylyl cyclase or phospholipase C 1061
In the kidney, PTH promotes Ca2+ reabsorption, phosphate loss, and 1-hydroxylation of 25-hydroxyvitamin D 1061
Stimulation of Ca2+ Reabsorption 1062
Inhibition of Phosphate Reabsorption 1062
Stimulation of the Last Step of Synthesis of 1,25- Dihydroxyvitamin D 1062
In bone, PTH can promote net resorption or net deposition 1063
Bone Resorption by Indirect Stimulation of Osteoclasts 1063
Bone Resorption by Reduction in Bone Matrix 1063
Bone Deposition 1063
Vitamin D 1063
The active form of vitamin D is its 1,25-dihydroxy metabolite 1063
Vitamin D, by acting on the small intestine and kidney, raises plasma [Ca2+] and thus promotes bone mineralization 1065
Small Intestine 1065
Kidney 1065
Bone 1065
Calcium ingestion lowers—whereas phosphate ingestion raises—levels of both PTH and 1,25-dihydroxyvitamin D 1067
Calcium Ingestion 1067
Phosphate Ingestion 1067
Calcitonin and Other Hormones 1067
Calcitonin inhibits osteoclasts, but its effects are transitory 1067
Sex steroid hormones promote bone deposition, whereas glucocorticoids promote resorption 1068
PTHrP, encoded by a gene that is entirely distinct from that for PTH, can cause hypercalcemia in certain malignancies 1069
References 1069
References 1069.e2
Books and Reviews 1069.e2
Journal Articles 1069.e2
IX The Reproductive System 1071
53 Sexual Differentiation 1072
Genetic Aspects of Sexual Differentiation 1072
Meiosis occurs only in germ cells and gives rise to male and female gametes 1072
Fertilization of an oocyte by an X- or Y-bearing sperm establishes the zygote’s genotypic sex 1073
Genotypic sex determines differentiation of the indifferent gonad into either an ovary or a testis 1075
The testis-determining gene is located on the Y chromosome 1075
Endocrine and paracrine messengers modulate phenotypic differentiation 1076
Differentiation of the Gonads 1076
Primordial germ cells migrate from the yolk sac to the primordial gonad 1076
The primitive testis develops from the medulla of the primordial gonad 1078
The primitive ovary develops from the cortex of the primordial gonad 1078
Development of the Accessory Sex Organs 1078
The embryonic gonad determines the development of the internal genitalia and the external sexual phenotype 1078
Embryos of both sexes have a double set of embryonic genital ducts 1078
In males, the wolffian ducts become the epididymis, vas deferens, seminal vesicles, and ejaculatory duct 1079
In females, the müllerian ducts become the fallopian tubes, the uterus, and the upper third of the vagina 1080
In males, development of the wolffian ducts requires testosterone 1080
In males, antimüllerian hormone causes regression of the müllerian ducts 1080
Differentiation of the External Genitalia 1081
The urogenital sinus develops into the urinary bladder, the urethra, and, in females, the vestibule of the vagina 1081
The external genitalia of both sexes develop from common anlagen 1083
Endocrine and Paracrine Control of Sexual Differentiation 1084
The SRY gene triggers development of the testis, which makes the androgens and AMH necessary for male sexual differentiation 1084
Testosterone Production 1085
Androgen Receptor 1085
DHT Formation 1085
Antimüllerian Hormone 1085
Androgens direct the male pattern of sexual differentiation of the internal ducts, the urogenital sinus, and the external genitalia 1085
Differentiation of the Duct System 1086
Differentiation of the Urogenital Sinus and External Genitalia 1086
Androgens and estrogens influence sexual differentiation of the brain 1086
Puberty 1087
Puberty involves steroid hormones produced by the gonads and the adrenals 1087
Hypothalamic gonadotropin-releasing hormone secretion controls puberty 1088
Multiple factors control the timing of puberty 1088
Androgens and estrogens influence secondary sex characteristics at puberty 1088
Males 1088
Females 1090
The appearance of secondary sex characteristics at puberty completes sexual differentiation and development 1091
References 1091
References 1091.e1
Books and Reviews 1091.e1
Journal Articles 1091.e1
54 The Male Reproductive System 1092
Hypothalamic-Pituitary-Gonadal Axis 1092
The hypothalamus secretes GnRH, which acts on gonadotrophs in the anterior pituitary 1092
Under the control of GnRH, gonadotrophs in the anterior pituitary secrete LH and FSH 1094
LH stimulates the Leydig cells of the testis to produce testosterone 1095
FSH stimulates Sertoli cells to synthesize hormones that influence Leydig cells and spermatogenesis 1095
The hypothalamic-pituitary-testicular axis is under feedback inhibition by testicular steroids and inhibins 1096
Testosterone 1097
Leydig cells convert cholesterol to testosterone 1097
Adipose tissue, skin, and the adrenal cortex also produce testosterone and other androgens 1097
Testosterone acts on target organs by binding to a nuclear receptor 1099
Metabolism of testosterone occurs primarily in the liver and prostate 1099
Biology of Spermatogenesis and Semen 1100
Spermatogenesis includes mitotic divisions of spermatogonia, meiotic divisions of spermatocytes to spermatids, and maturation to spermatozoa N54-7 1100
The Sertoli cells support spermatogenesis 1100
Sperm maturation occurs in the epididymis 1102
Spermatozoa are the only independently motile cells in the human body 1103
The accessory male sex glands—the seminal vesicles, prostate, and bulbourethral glands—produce the seminal plasma 1103
Male Sex Act 1104
The sympathetic and parasympathetic divisions of the autonomic nervous system control the male genital system 1104
Sympathetic Division of the ANS 1104
Parasympathetic Division of the ANS 1104
Visceral Afferents 1105
Erection is primarily under parasympathetic control 1105
Parasympathetic Innervation 1106
Sympathetic Innervation 1106
Somatic Innervation 1106
Afferent Innervation 1106
Emission is primarily under sympathetic control 1106
Motor Activity of the Duct System 1107
Secretory Activity of the Accessory Glands 1107
Ejaculation is under the control of a spinal reflex 1107
References 1107
References 1107.e2
Books and Reviews 1107.e2
Journal Articles 1107.e2
55 The Female Reproductive System 1108
Female reproductive organs include the ovaries and accessory sex organs 1108
Reproductive function in the human female is cyclic 1108
Hypothalamic-Pituitary-Gonadal Axis and Control of the Menstrual Cycle 1110
The human menstrual cycle coordinates changes in both the ovary and endometrium 1110
Follicular/Proliferative Phase 1110
Ovulation 1111
Luteal/Secretory Phase 1111
Menses 1111
The hypothalamic-pituitary-ovarian axis drives the menstrual cycle 1111
Neurons in the hypothalamus release GnRH in a pulsatile fashion 1111
GnRH stimulates gonadotrophs in the anterior pituitary to secrete FSH and LH 1111
The ovarian steroids (estrogens and progestins) feed back on the hypothalamic-pituitary axis 1112
Negative Feedback by Ovarian Steroids 1112
Positive Feedback by Ovarian Steroids 1113
Ovaries produce peptide hormones—inhibins, activins, and follistatins—that modulate FSH secretion 1113
Negative Feedback by the Inhibins 1114
Positive Feedback by the Activins 1114
Modulation of gonadotropin secretion by positive and negative ovarian feedback produces the normal menstrual rhythm 1115
Ovarian Steroids 1116
Starting from cholesterol, the ovary synthesizes estradiol, the major estrogen, and progesterone, the major progestin 1116
Estrogen biosynthesis requires two ovarian cells and two gonadotropins, whereas progestin synthesis requires only a single cell 1117
Estrogens stimulate cellular proliferation and growth of sex organs and other tissues related to reproduction 1119
The Ovarian Cycle: Folliculogenesis, Ovulation, and Formation of the Corpus Luteum 1120
Female reproductive life span is determined by the number of primordial follicles established during fetal life 1120
Primary Oocytes 1120
Primordial Follicles 1121
Primary Follicles 1122
Secondary Follicles 1122
Tertiary Follicles 1122
Graafian Follicles 1122
The oocyte grows and matures during folliculogenesis 1122
FSH and LH stimulate the growth of a cohort of follicles 1122
Each month, one follicle achieves dominance 1123
Estradiol secretion by the dominant follicle triggers the LH surge and thus ovulation 1123
After ovulation, theca and granulosa cells of the follicle differentiate into theca-lutein and granulosa-lutein cells of the corpus luteum 1124
Growth and involution of the corpus luteum produce the rise and fall in estradiol and progesterone during the luteal phase 1124
The Endometrial Cycle 1124
The ovarian hormones drive the morphological and functional changes of the endometrium during the monthly cycle 1124
The Menstrual Phase 1124
The Proliferative Phase 1124
The Secretory Phase 1125
The effective implantation window is 3 to 4 days 1126
Female Sex Act 1126
The female sex response occurs in four distinct phases 1126
Excitement 1126
Plateau 1127
Orgasm 1127
Resolution 1127
Both the sympathetic and the parasympathetic divisions control the female sex response 1127
The female sex response facilitates sperm transport through the female reproductive tract 1127
Menopause 1127
Only a few functioning follicles remain in the ovaries of a menopausal woman 1127
During menopause, levels of the ovarian steroids fall, whereas gonadotropin levels rise 1128
References 1128
References 1128.e1
Books and Reviews 1128.e1
Journal Articles 1128.e1
56 Fertilization, Pregnancy, and Lactation 1129
Transport of Gametes and Fertilization 1129
Cilia and smooth muscle transport the egg and sperm within the female genital tract 1129
The “capacitation” of the spermatozoa that occurs in the female genital tract enhances the ability of the sperm cell to fertilize the ovum 1129
Fertilization begins as the sperm cell attaches to the zona pellucida and undergoes the acrosomal reaction, and it ends with the fusion of the male and female pronuclei 1129
Implantation of the Developing Embryo 1132
The presence of an embryo leads to decidualization of the endometrium 1133
Uterine secretions nourish the preimplantation embryo, promote growth, and prepare it for implantation 1133
The blastocyst secretes substances that facilitate implantation 1133
During implantation, the blastocyst apposes itself to the endometrium, adheres to epithelial cells, and finally invades the stroma 1134
Apposition 1134
Adhesion 1135
Invasion 1136
Physiology of the Placenta 1136
At the placenta, the space between the fetus’s chorionic villi and the mother’s endometrial wall contains a continuously renewed pool of extravasated maternal blood 1136
Maternal Blood Flow 1136
Fetal Blood Flow 1137
Gases and other solutes move across the placenta 1137
O2 and CO2 Transport 1137
Other Solutes 1138
The placenta makes a variety of peptide hormones, including hCG and human chorionic somatomammotropin 1139
The Maternal-Placental-Fetal Unit 1139
During pregnancy, progesterone and estrogens rise to levels that are substantially higher than their peaks in a normal cycle 1139
After 8 weeks of gestation, the maternal-placental-fetal unit maintains high levels of progesterone and estrogens 1140
Response of the Mother to Pregnancy 1142
Both maternal cardiac output and blood volume increase during pregnancy 1142
Increased levels of progesterone during pregnancy increase alveolar ventilation 1143
Pregnancy increases the demand for dietary protein, iron, and folic acid 1143
Less than one third of the total maternal weight gain during pregnancy represents the fetus 1143
Parturition 1144
Human birth usually occurs at around the 40th week of gestation 1144
Parturition occurs in distinct stages, numbered 0 to 3 1144
Stage 0—Quiescence 1144
Stage 1—Transformation/Activation 1144
Stage 2—Active Labor 1144
Stage 3—Involution 1144
Reciprocal decreases in progesterone receptors and increases in estrogen receptors are critical for the onset of labor 1144
Signals from the fetus may initiate labor 1145
PGs initiate uterine contractions, and both PGs and OT sustain labor 1145
Prostaglandins 1145
Oxytocin 1145
Relaxin 1146
Mechanical Factors 1146
Positive Feedback 1146
Lactation 1146
The epithelial alveolar cells of the mammary gland secrete the complex mixture of sugars, proteins, lipids, and other substances that constitute milk 1146
PRL is essential for milk production, and suckling is a powerful stimulus for PRL secretion 1148
OT and psychic stimuli initiate milk ejection (“let-down”) 1150
Suckling inhibits the ovarian cycle 1150
References 1150
References 1150.e1
Books and Reviews 1150.e1
Journal Articles 1150.e1
57 Fetal and Neonatal Physiology 1151
Biology of Fetal Growth 1151
Two distinct circulations—fetoplacental and uteroplacental—underlie the transfer of gases and nutrients 1151
Growth occurs by hyperplasia and hypertrophy 1151
Growth depends primarily on genetic factors during the first half of gestation and on epigenetic factors thereafter 1152
Increases in placental mass parallel periods of rapid fetal growth 1152
Insulin, the insulin-like growth factors, and thyroxine stimulate fetal growth 1153
Glucocorticoids and Insulin 1153
Insulin-Like Growth Factors 1154
Epidermal Growth Factor 1154
Thyroid Hormones 1154
Peptide Hormones 1154
Many fetal tissues produce red blood cells early in gestation 1154
The fetal gastrointestinal and urinary systems excrete products into the amniotic fluid by midpregnancy 1154
A surge in protein synthesis, with an increase in muscle mass, is a major factor in the rapid fetal weight gain during the third trimester 1155
Fetal lipid stores increase rapidly during the third trimester 1155
Development and Maturation of the Cardiopulmonary System 1155
Fetal lungs develop by repetitive branching of both bronchial and pulmonary arterial trees 1155
An increase in cortisol, with other hormones, triggers surfactant production in the third trimester 1156
Fetal respiratory movements begin near the end of the first trimester but wane just before birth 1157
The fetal circulation has four unique pathways—placenta, ductus venosus, foramen ovale, and ductus arteriosus—to facilitate gas and nutrient exchange 1157
Placenta 1158
Ductus Venosus 1158
Foramen Ovale 1158
Ductus Arteriosus 1158
Cardiopulmonary Adjustments at Birth 1159
Loss of the placental circulation requires the newborn to breathe on its own 1159
Mild hypoxia and hypercapnia, as well as tactile stimuli and cold skin, trigger the first breath 1159
At birth, removal of the placenta increases systemic vascular resistance, whereas lung expansion decreases pulmonary vascular resistance 1162
Removal of the Placental Circulation 1162
Increase in Pulmonary Blood Flow 1162
Closure of the ductus venosus within the first days of life forces portal blood to perfuse the liver 1162
Closure of the foramen ovale occurs as left atrial pressure begins to exceed right atrial pressure 1162
Closure of the ductus arteriosus completes the separation between the pulmonary and systemic circulations 1163
Neonatal Physiology 1164
Although the newborn is prone to hypothermia, nonshivering thermogenesis in brown fat helps to keep the neonate warm 1164
The neonate mobilizes glucose and FAs soon after delivery 1166
Carbohydrate Metabolism 1166
Fat Metabolism 1166
Metabolic Rate 1166
Breast milk from a mother with a balanced diet satisfies all of the infant’s nutritional requirements during the first several months of life 1166
The neonate is at special risk of developing fluid and acid-base imbalances 1167
Humoral and cellular immune responses begin at early stages of development in the fetus 1167
Fetus 1167
Neonate 1167
In premature newborns, immaturity of organ systems and fragility of homeostatic mechanisms exacerbate postnatal risks 1168
References 1168
References 1168.e2
Books and Reviews 1168.e2
Journal Articles 1168.e2
X Physiology of Everyday Life 1169
58 Metabolism 1170
Forms of Energy 1170
Energy Balance 1172
Energy input to the body is the sum of energy output and storage 1172
The inefficiency of chemical reactions leads to loss of the energy available for metabolic processes 1173
Free energy, conserved as high-energy bonds in ATP, provides the energy for cellular functions 1174
Energy Interconversion From Cycling between 6-Carbon and 3-Carbon Molecules 1174
Glycolysis converts the 6-carbon glucose molecule to two 3-carbon pyruvate molecules 1174
Gluconeogenesis converts nonhexose precursors to the 6-carbon glucose molecule 1176
Reciprocal regulation of glycolysis and gluconeogenesis minimizes futile cycling 1178
Allosteric Regulation 1178
Transcriptional Regulation 1178
Cells can convert glucose or amino acids into FAs 1178
The body permits only certain energy interconversions 1179
Energy Capture (Anabolism) 1179
After a carbohydrate meal, the body burns some ingested glucose and incorporates the rest into glycogen or TAGs 1179
Liver 1179
Muscle 1181
Adipose Tissue 1181
After a protein meal, the body burns some ingested amino acids and incorporates the rest into proteins 1181
After a fatty meal, the body burns some ingested FAs and incorporates the rest into TAGs 1182
Energy Liberation (Catabolism) 1182
The first step in energy catabolism is to break down glycogen or TAGs to simpler compounds 1182
Skeletal Muscle 1182
Liver 1182
Adipocytes 1182
The second step in TAG catabolism is β-oxidation of FAs 1183
The final common steps in oxidizing carbohydrates, TAGs, and proteins to CO2 are the citric acid cycle and oxidative phosphorylation 1185
Citric Acid Cycle 1185
Oxidative Phosphorylation 1185
Ketogenesis 1185
Oxidizing different fuels yields similar amounts of energy per unit O2 consumed 1187
Integrative Metabolism During Fasting 1188
During an overnight fast, glycogenolysis and gluconeogenesis maintain plasma glucose levels 1189
Requirement for Glucose 1189
Gluconeogenesis versus Glycogenolysis 1189
Gluconeogenesis: The Cori Cycle 1189
Gluconeogenesis: The Glucose-Alanine Cycle 1189
Lipolysis 1190
Starvation beyond an overnight fast enhances gluconeogenesis and lipolysis 1190
Enhanced Gluconeogenesis 1190
Enhanced Lipolysis 1191
Prolonged starvation moderates proteolysis but accelerates lipolysis, thereby releasing ketone bodies 1191
Decreased Proteolysis 1191
Decreased Hepatic Gluconeogenesis 1191
Increased Renal Gluconeogenesis 1191
Increased Lipolysis and Ketogenesis 1191
References 1192
References 1192.e1
Books and Reviews 1192.e1
Journal Articles 1192.e1
59 Regulation of Body Temperature 1193
Heat and Temperature: Advantages of Homeothermy 1193
Homeotherms maintain their activities over a wide range of environmental temperatures 1193
Body core temperature depends on time of day, physical activity, time in the menstrual cycle, and age 1193
The body’s rate of heat production can vary from ~70 kcal/hr at rest to 600 kcal/hr during exercise 1194
Modes of Heat Transfer 1194
Maintaining a relatively constant body temperature requires a fine balance between heat production and heat losses 1194
Heat moves from the body core to the skin, primarily by convection 1195
Heat moves from the skin to the environment by radiation, conduction, convection, and evaporation 1196
Radiation 1196
Conduction 1196
Convection 1197
Evaporation 1197
When heat gain exceeds heat loss, body core temperature rises 1197
Clothing insulates the body from the environment and limits heat transfer from the body to the environment 1198
Active Regulation of Body Temperature by the Central Nervous System 1198
Thermoreceptors in the skin and temperature-sensitive neurons in the hypothalamus respond to changes in their local temperature 1198
Skin Thermoreceptors 1198
Hypothalamic Temperature-Sensitive Neurons 1199
The CNS thermoregulatory network integrates thermal information and directs changes in efferent activity to modify rates of heat transfer and production 1200
Thermal effectors include behavior, cutaneous circulation, sweat glands, and skeletal muscles responsible for shivering 1200
Hypothermia, Hyperthermia, and Fever 1201
Hypothermia or hyperthermia occurs when heat transfer to or from the environment overwhelms the body’s thermoregulatory capacity 1201
Exercise raises heat production, which is followed by a matching rise in heat loss, but at the cost of a steady-state hyperthermia of exercise 1202
Fever is a regulated hyperthermia 1202
References 1203
References 1203.e2
Books and Reviews 1203.e2
Journal Articles 1203.e2
60 Exercise Physiology and Sports Science 1204
Motor Units and Muscle Function 1204
The motor unit is the functional element of muscle contraction 1204
Muscle force rises with the recruitment of motor units and an increase in their firing frequency 1204
Compared with type I motor units, type II units are faster and stronger but more fatigable 1205
As external forces stretch muscle, series elastic elements contribute a larger fraction of total tension 1206
The action of a muscle depends on the axis of its fibers and its origin and insertion on the skeleton 1207
Fluid and energetically efficient movements require learning 1207
Strength versus endurance training differentially alters the properties of motor units N60-3 1208
Conversion of Chemical Energy to Mechanical Work 1208
ATP and PCr provide immediate but limited energy 1208
Anaerobic glycolysis provides a rapid but self-limited source of ATP 1209
Oxidation of glucose, lactate, and fatty acids provides a slower but long-term source of ATP 1209
Oxidation of Nonmuscle Glucose 1209
Oxidation of Lactate 1211
Gluconeogenesis 1211
Oxidation of Nonmuscle Lipid 1211
Choice of Fuel Sources 1211
Muscle Fatigue 1212
Fatigued muscle produces less force and has a reduced velocity of shortening 1212
Changes in the CNS produce central fatigue 1212
Impaired excitability and impaired Ca2+ release can produce peripheral fatigue 1212
High-Frequency Fatigue 1212
Low-Frequency Fatigue 1212
Fatigue can result from ATP depletion, lactic acid accumulation, and glycogen depletion 1213
ATP Depletion 1213
Lactic Acid Accumulation 1213
Glycogen Depletion 1213
Determinants of Maximal O2 Uptake and Consumption 1213
Maximal O2 uptake by the lungs can exceed resting O2 uptake by more than 20-fold 1213
O2 uptake by muscle is the product of muscle blood flow and O2 extraction 1214
O2 delivery by the cardiovascular system is the limiting step for maximal O2 utilization 1214
Limited O2 Uptake by the Lungs 1214
Limited O2 Delivery by the Cardiovascular System 1214
Limited O2 Extraction by Muscle 1215
Effective circulating volume takes priority over cutaneous blood flow for thermoregulation 1215
Sweating 1215
Eccrine, but not apocrine, sweat glands contribute to temperature regulation 1215
Eccrine sweat glands are tubules comprising a secretory coiled gland and a reabsorptive duct 1216
Secretion by Coil Cells 1218
Reabsorption by Duct Cells 1218
The NaCl content of sweat increases with the rate of secretion but decreases with acclimatization to heat 1218
Flow Dependence 1218
Cystic Fibrosis 1218
Replenishment 1218
Acclimatization 1219
The hyperthermia of exercise stimulates eccrine sweat glands 1219
Endurance (Aerobic) Training 1219
Aerobic training requires regular periods of stress and recovery 1219
Aerobic training increases maximal O2 delivery by increasing plasma volume and maximal cardiac output 1219
Maximizing Arterial O2 Content 1219
Maximizing Cardiac Output 1220
Aerobic training enhances O2 diffusion into muscle 1220
Aerobic training increases mitochondrial content 1220
References 1222
References 1222.e1
Books and Reviews 1222.e1
Journal Articles 1222.e1
61 Environmental Physiology 1223
The Environment 1223
Voluntary feedback control mechanisms can modulate the many layers of our external environment 1223
Environmental temperature provides conscious clues for triggering voluntary feedback mechanisms 1224
Room ventilation should maintain , , and levels of toxic substances within acceptable limits 1224
Acceptable Limits for and 1224
Measuring Room Ventilation 1224
Carbon Monoxide 1224
Threshold Limit Values and Biological Exposure Indices 1225
Tissues must resist the G force produced by gravity and other mechanisms of acceleration 1225
The partial pressures of gases—other than water—inside the body depend on Pb 1225
Diving Physiology 1225
Immersion raises Pb, thereby compressing gases in the lungs 1225
SCUBA divers breathe compressed air to maintain normal lung expansion 1226
Increased alveolar can cause narcosis 1227
Increased alveolar can lead to O2 toxicity 1227
Using helium to replace inspired N2 and O2 avoids nitrogen narcosis and O2 toxicity 1228
After an extended dive, one must decompress slowly to avoid decompression illness 1229
High-Altitude Physiology 1230
Pb and ambient on top of Mount Everest are approximately one third of their values at sea level 1230
Everest Base Camp 1230
Peak of Mount Everest 1230
Air Travel 1230
Up to modest altitudes, arterial O2 content falls relatively less than Pb due to the shape of the Hb-O2 dissociation curve 1230
During the first few days at altitude, compensatory adjustments to hypoxemia include tachycardia and hyperventilation 1231
Long-term adaptations to altitude include increases in hematocrit, pulmonary diffusing capacity, capillarity, and oxidative enzymes 1231
Hematocrit 1231
Pulmonary Diffusing Capacity 1232
Capillary Density 1232
Oxidative Enzymes 1232
High altitude causes mild symptoms in most people and acute or chronic mountain sickness in susceptible individuals 1232
Symptoms of Hypoxia 1232
Acute Mountain Sickness 1232
Chronic Mountain Sickness 1232
Flight and Space Physiology 1232
Acceleration in one direction shifts the blood volume in the opposite direction 1232
“Weightlessness” causes a cephalad shift of the blood volume and an increase in urine output 1233
Space flight leads to motion sickness and to decreases in muscle and bone mass 1233
Exercise partially overcomes the deconditioning of muscles during space flight 1234
Return to earth requires special measures to maintain arterial blood pressure 1234
References 1234
References 1234.e1
Books and Reviews 1234.e1
Journal Articles 1234.e1
62 The Physiology of Aging 1235
Concepts in Aging 1235
During the 20th century, the age structure of populations in developed nations shifted toward older individuals 1235
The definition, occurrence, and measurement of aging are fundamental but controversial issues 1235
Aging is an evolved trait 1235
Human aging studies can be cross-sectional or longitudinal 1237
Cross-Sectional Design 1237
Longitudinal Design 1237
Whether age-associated diseases are an integral part of aging remains controversial 1237
Cellular and Molecular Mechanisms of Aging 1238
Oxidative stress and related processes that damage macromolecules may have a causal role in aging 1238
Reactive Oxygen Species 1238
Glycation and Glycoxidation 1239
Mitochondrial Damage 1239
Somatic Mutations 1239
Inadequacy of repair processes may contribute to the aging phenotype 1240
DNA Repair 1240
Protein Homeostasis 1240
Autophagy 1240
Dysfunction of the homeostasis of cell number may be a major factor in aging 1240
Limitations in Cell Division 1240
Cell Removal 1241
Aging of the Human Physiological Systems 1242
Aging people lose height and lean body mass but gain and redistribute fat 1243
Aging thins the skin and causes the musculoskeletal system to become weak, brittle, and stiff 1243
Skin 1243
Skeletal Muscle 1243
Bone 1243
Synovial Joints 1243
The healthy elderly experience deficits in sensory transduction and speed of central processing 1244
Sensory Functions 1244
Motor Functions 1244
Cognitive Functions 1244
Aging causes decreased arterial compliance and increased ventilation-perfusion mismatching 1244
Cardiovascular Function 1244
Pulmonary Function 1244
Exercise 1244
Glomerular filtration rate falls with age in many but not all people 1245
Aging has only minor effects on gastrointestinal function 1245
Aging causes modest declines in most endocrine functions 1245
Insulin 1245
Growth Hormone and IGF-1 1245
Adrenal Steroids 1245
Thyroid Hormones 1245
Parathyroid Hormone 1245
Gonadal Hormones 1245
Aging Slowly 1246
Caloric restriction slows aging and extends life in several species, including some mammals 1246
Genetic alterations can extend life in several species 1246
Proposed interventions to slow aging and extend human life are controversial 1247
References 1247
References 1247.e1
Books and Reviews 1247.e1
Journal Articles 1247.e1
Index 1249
Numbers 1249
A 1249
B 1252
C 1255
D 1259
E 1261
F 1264
G 1266
H 1269
I 1271
J 1272
K 1273
L 1273
M 1274
N 1277
O 1279
P 1280
Q 1286
R 1286
S 1288
T 1292
U 1295
V 1295
W 1296
X 1296
Y 1296
Z 1296