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Co-Director, University of California, Davis School of Medicine

This result demonstrates convincingly that the early inward current measured when Na+ is present in the external medium must be due to Na+ entering the neuron. This further result shows that the late outward current must be due to the flow of an ion other than Na+. Several lines of evidence presented by Hodgkin, Huxley, and others showed that this late outward current is caused by K+ exiting the neuron. Perhaps the most compelling demonstration of K+ involvement is that the amount of K+ efflux from the neuron, measured by loading the neuron with radioactive K+, is closely correlated with the magnitude of the late outward current. Taken together, these experiments using the voltage clamp show that changing the membrane potential to a level more positive than the resting potential produces two effects: an early influx of Na+ into the neuron, followed by a delayed efflux of K+. The early influx of Na+ produces a transient inward current, whereas the delayed efflux of K+ produces a sustained outward current. The differences in the time course and ionic selectivity of the two fluxes suggest that two different ionic permeability mechanisms are activated by changes in membrane potential. Confirmation that there are indeed two distinct mechanisms has come from pharmacological studies of drugs that specifically affect these two currents (Figure 3. Tetrodotoxin, an alkaloid neurotoxin found in certain puffer fish, tropical frogs, and salamanders, blocks the Na+ current without affecting the K+ current. Conversely, tetraethylammonium ions block K+ currents without affecting Na+ currents. The differential sensitivity of Na+ and K+ currents to these drugs provides strong additional evidence that Na+ and K+ flow through independent permeability pathways. As discussed in Chapter 4, it is now known that these pathways are ion channels that are selectively permeable to either Na+ or K+. In fact, tetrodotoxin, tetraethylammonium, and other drugs that interact with spe- + + 460 mM Na+ 0 Early current is inward Membrane current (mA/cm2) -1 +1 Na+-free 0 Early current is outward -1 +1 460 mM Na+ 0 Early current is inward again -1 0 2 4 Time (ms) 6 8 52 Chapter Three Figure 3. Panel (1) shows the current that flows when the membrane potential of a squid axon is depolarized to 0 mV in control conditions. Two Voltage-Dependent Membrane Conductances the next goal Hodgkin and Huxley set for themselves was to describe Na+ and K+ permeability changes mathematically. To do this, they assumed that the ionic currents are due to a change in membrane conductance, defined as the reciprocal of the membrane resistance. Membrane conductance is thus closely related, although not identical, to membrane permeability. When evaluating ionic movements from an electrical standpoint, it is convenient to describe them in terms of ionic conductances rather than ionic permeabilities. The difference between Vm and Eion is the electrochemical driving force acting on the ion. Hodgkin and Huxley used this simple relationship to calculate the dependence of Na+ and K+ conductances on time and membrane potential. From these measurements, Hodgkin and Huxley were able to calculate gNa and gK (Figure 3. For example, both Na+ and K+ conductances require some time to activate, or turn on. In particular, the K+ conductance has a pronounced delay, requiring several milliseconds to reach its maximum (Figure 3. The more rapid activation of the Na+ conductance allows the resulting inward Na+ current to precede the delayed outward K+ current (see Figure 3. Although the Na+ conductance rises rapidly, it quickly declines, even though the membrane potential is kept at a depolarized level. This fact shows that depolarization not only causes the Na+ conductance to activate, but also causes it to decrease over time, or inactivate. The K+ conductance of the squid axon does not inactivate in this way; thus, while the Na+ and K+ conductances share the property of time-dependent activation, only the Na+ conductance inactivates. Depolarizations to various membrane potentials (A) elicit different membrane currents (B). Below are shown the Na+ (C) and K+ (D) conductances calculated from these currents.

The pericardial sac normally contains 5-30 mL of clear fluid, which lubricates the heart and permits it to contract with minimal friction. Timing Although events on the two sides of the heart are similar, they are somewhat asynchronous. Right atrial systole precedes left atrial systole, and contraction of the right ventricle starts after that of the left (see Chapter 28). However, since pulmonary arterial pressure is lower than aortic pressure, right ventricular ejection begins before left ventricular ejection. During expiration, the pulmonary and aortic valves close at the same time; but during inspiration, the aortic valve closes slightly before the pulmonary. The slower closure of the pulmonary valve is due to lower impedance of the pulmonary vascular tree. When measured over a period of minutes, the outputs of the two ventricles are, of course, equal, but transient differences in output during the respiratory cycle occur in normal individuals. Length of Systole & Diastole Cardiac muscle has the unique property of contracting and repolarizing faster when the heart rate is high (see Chapter 3), and the duration of systole decreases from 0. However, the duration of systole is much more fixed than that of diastole, and when the heart rate is increased, diastole is shortened to a much greater degree. It is during diastole that the heart muscle rests, and coronary blood flow to the subendocardial portions of the left ventricle occurs only during diastole (see Chapter 32). At heart rates up to about 180, filling is adequate as long as there is ample venous return, and cardiac output per minute is increased by an increase in rate. However, at very high heart rates, filling may be compromised to such a degree that cardiac output per minute falls and symptoms of heart failure develop. Because it has a prolonged action potential, cardiac muscle is in its refractory period and will not contract in response to a second stimulus until near the end of the initial contraction (see Figure 3-14). A ventricular rate of more than 230 is seen only in paroxysmal ventricular tachycardia (see Chapter 28). Arterial Pulse the blood forced into the aorta during systole not only moves the blood in the vessels forward but also sets up a pressure wave that travels along the arteries. The pressure wave expands the arterial walls as it travels, and the expansion is palpable as the pulse. The rate at which the wave travels, which is independent of and much higher than the velocity of blood flow, is about 4 m/s in the aorta, 8 m/s in the large arteries, and 16 m/s in the small arteries of young adults. With advancing age, the arteries become more rigid, and the pulse wave moves faster. The strength of the pulse is determined by the pulse pressure and bears little relation to the mean pressure. It is strong when stroke volume is large, eg, during exercise or after the administration of histamine. When the pulse pressure is high, the pulse waves may be large enough to be felt or even heard by the individual (palpitation, "pounding heart"). When the aortic valve is incompetent (aortic insufficiency), the pulse is particularly strong, and the force of systolic ejection may be sufficient to make the head nod with each heartbeat. The pulse in aortic insufficiency is called a collapsing, Corrigan, or water-hammer pulse. A water hammer is an evacuated glass tube half-filled with water that was a popular toy in the 19th century. The dicrotic notch, a small oscillation on the falling phase of the pulse wave caused by vibrations set up when the aortic valve snaps shut (Figure 29-3), is visible if the pressure wave is recorded but is not palpable at the wrist. There is also a dicrotic notch on the pulmonary artery pressure curve produced by the closure of the pulmonary valves. The atrial pressure changes are transmitted to the great veins, producing three characteristic waves in the record of jugular pressure (Figure 29-3). As noted above, some blood regurgitates into the great veins when the atria contract, even though the orifices of the great veins are constricted. In addition, venous inflow stops, and the resultant rise in venous pressure contributes to the a wave. The c wave is the transmitted manifestation of the rise in atrial pressure produced by the bulging of the tricuspid valve into the atria during isovolumetric ventricular contraction.

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The total body osmolality is directly proportionate to the total body sodium plus the total body potassium divided by the total body water, so that changes in the osmolality of the body fluids occur when there is a disproportion between the amount of these electrolytes and the amount of water ingested or lost from the body (see Chapter 1). When the effective osmotic pressure of the plasma rises, vasopressin secretion is increased and the thirst mechanism is stimulated. Water is retained in the body, diluting the hypertonic plasma, and water intake is increased (Figure 39-1). Conversely, when the plasma becomes hypotonic, vasopressin secretion is decreased and "solute-free water" (water in excess of solute) is excreted. In this way, the tonicity of the body fluids is maintained within a narrow normal range. In health, plasma osmolality ranges from 280 to 295 mosm/kg of H2O, with vasopressin secretion maximally inhibited at 285 mosm/kg and stimulated at higher values (see Figure 14-14). The details of the way the regulatory mechanisms operate and the disorders that result when their function is disrupted are considered in Chapters 14 and 38. It also causes thirst and constricts blood vessels, which help to maintain blood pressure. The immediate compensations in shock operate principally to maintain intravascular volume (see Chapter 33), but they also affect Na+ balance. Because of the key position of Na+ in volume homeostasis, it is not surprising that more than one mechanism has evolved to control the excretion of this ion. The filtration and reabsorption of Na + in the kidneys and the effects of these processes on Na + excretion are discussed in Chapter 38. Tubular reabsorption of Na + is increased, in part because the secretion of aldosterone is increased. Aldosterone secretion is controlled in part by a feedback system in which the change that initiates increased secretion is a decline in mean intravascular pressure (see Chapters 20 and 24). Other changes in Na + excretion occur too rapidly to be due solely to changes in aldosterone secretion. For example, rising from the supine to the standing position increases aldosterone secretion. However, Na+ excretion is decreased within a few minutes, and this rapid change in Na + excretion occurs in adrenalectomized subjects. The Mg2+ concentration is subject to close regulation, but the mechanisms controlling Mg+ metabolism are incompletely understood. Intracellular H+ concentration, which can be measured by using microelectrodes, pH-sensitive fluorescent dyes, and phosphorus magnetic resonance, is different from extracellular pH and appears to regulate a variety of intracellular processes. The pH notation is a useful means of expressing H+ concentrations in the body, because the H + concentrations happen to be low relative to those of other cations. Thus, the normal Na + concentration of arterial plasma that has been equilibrated with red blood cells is about 140 meq/L, whereas the H + concentration is 0. It is important to remember that the pH of blood is the pH of true plasma-plasma that has been in equilibrium with red cells-because the red cells contain hemoglobin, which is quantitatively one of the most important blood buffers (see Chapter 35). Failure of diseased kidneys to excrete normal amounts of acid is also a cause of acidosis. This is why the most effective buffers in the body would be expected to be those with pKs close to the pH in which they operate. It should be noted that the equilibrium constant, K, applies only to infinitely dilute solutions in which interionic forces are negligible. Buffers in Blood In the blood, proteins-particularly the plasma proteins-are effective buffers because both their free carboxyl and their free amino groups dissociate: Another important buffer system is provided by the dissociation of the imidazole groups of the histidine residues in hemoglobin: In the pH 7. However, the hemoglobin molecule contains 38 histidine residues, and on this basis-plus the fact that hemoglobin is present in large amounts-the hemoglobin in blood has six times the buffering capacity of the plasma proteins. In addition, the action of hemoglobin is unique because the imidazole groups of deoxyhemoglobin dissociate less than those of oxyhemoglobin, making Hb a weaker acid and therefore a better buffer than HbO 2. There is no carbonic anhydrase in plasma, but there is an abundant supply in red blood cells. It is also found in high concentration in gastric acid-secreting cells (see Chapter 26) and in renal tubular cells (see Chapter 38).

A portion of the posterior superior temporal gyrus known as the planum temporale (Figure 9-16) is regularly larger in the left than in the right cerebral hemisphere, particularly in right-handed individuals. A curious observation which is presently unexplained is that the planum temporale is even larger than normal on the left side, ie, the asymmetry is greater, in musicians and others who have perfect pitch. Sound Localization Determination of the direction from which a sound emanates in the horizontal plane depends upon detecting the difference in time between the arrival of the stimulus in the two ears and the consequent difference in phase of the sound waves on the two sides; it also depends upon the fact that the sound is louder on the side closest to the source. The detectable time difference, which can be as little as 20 us, is said to be the most important factor at frequencies below 3000 Hz and the loudness difference the most important at frequencies above 3000 Hz. Neurons in the auditory cortex that receive input from both ears respond maximally or minimally when the time of arrival of a stimulus at one ear is delayed by a fixed period relative to the time of arrival at the other ear. Sounds coming from directly in front of the individual differ in quality from those coming from behind, because each pinna (the visible portion of the exterior ear) is turned slightly forward. In addition, reflections of the sound waves from the pinnal surface change as sounds move up or down, and the change in the sound waves is the primary factor in locating sounds in the vertical plane. This device presents the subject with pure tones of various frequencies through earphones. At each frequency, the threshold intensity is determined and plotted on a graph as a percentage of normal hearing. This provides an objective measurement of the degree of deafness and a picture of the tonal range most affected. Deafness Clinical deafness may be due to impaired sound transmission in the external or middle ear (conduction deafness) or to damage to the hair cells or neural pathways (nerve deafness). Three of these tests, named for the men who developed them, are outlined in Table 9-1. The Weber and Schwabach tests demonstrate the important masking effect of environmental noise on the auditory threshold. Among the causes of conduction deafness are plugging of the external auditory canals with wax or foreign bodies, destruction of the auditory ossicles, thickening of the eardrum following repeated middle ear infections, and abnormal rigidity of the attachments of the stapes to the oval window. Aminoglycoside antibiotics such as streptomycin and gentamicin obstruct the mechanosensitive channels in the stereocilia of hair cells and can cause the cells to degenerate, producing nerve deafness and abnormal vestibular function. Damage to the outer hair cells by prolonged exposure to noise is associated with hearing loss. Other causes include tumors of the vestibulocochlear nerve and cerebellopontine angle, and vascular damage in the medulla. Presbycusis, the gradual hearing loss associated with aging, affects more than one-third of those over 75 and is probably due to gradual cumulative loss of hair cells and neurons. In 30% of the cases, it is associated with abnormalities in other systems (syndromic deafness), but in the remaining 70% it is the only apparent abnormality (nonsyndromic deafness). There is evidence that nonsyndromic deafness due to some mutations can first appear in adults rather than children, so the incidence is higher than 0. In the past few years, a remarkably large number of mutations that cause deafness have been described. This not only has added to knowledge about the pathophysiology of deafness, but characterization of the normal products of the genes has provided valuable information about the physiology of hearing. It is now estimated that the products of 100 or more genes are essential for normal hearing, and deafness loci have been described in all but five of the 24 human chromosomes. Interesting examples of proteins which when mutated cause deafness include connexin 26. The defect this produces in the function of connexons (see Chapter 1) presumably prevents the normal recycling of K + through the sustenacular cells (Figure 9-9). Deafness is also associated with mutant forms of a-tectin, one of the major proteins in the tectorial membrane. The endolymph, because of its inertia, is displaced in a direction opposite to the direction of rotation. When a constant speed of rotation is reached, the fluid spins at the same rate as the body and the cupula swings back into the upright position. When rotation is stopped, deceleration produces displacement of the endolymph in the direction of the rotation, and the cupula is deformed in a direction opposite to that during acceleration. Movement of the cupula in one direction commonly causes increased impulse traffic in single nerve fibers from its crista, whereas movement in the opposite direction commonly inhibits neural activity (Figure 9-17).