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Ganong's Review of Medical Physiology, 23rd Edition

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560 SECTION VI Cardiovascular <strong>Physiology</strong><br />

BARORECEPTOR NERVE ACTIVITY<br />

Baroreceptors are more sensitive to pulsatile pressure than to<br />

constant pressure. A decline in pulse pressure without any<br />

change in mean pressure decreases the rate <strong>of</strong> baroreceptor discharge<br />

and provokes a rise in systemic blood pressure and<br />

tachycardia. At normal blood pressure levels (about 100 mm Hg<br />

mean pressure), a burst <strong>of</strong> action potentials appears in a single<br />

baroreceptor fiber during systole, but there are few action potentials<br />

in early diastole (Figure 33–5). At lower mean pressures,<br />

this phasic change in firing is even more dramatic with<br />

activity only occurring during systole. At these lower pressures,<br />

the overall firing rate is considerably reduced. The<br />

threshold for eliciting activity in the carotid sinus nerve is<br />

about 50 mm Hg; maximal activity occurs at about 200 mm Hg.<br />

When one carotid sinus is isolated and perfused and the<br />

other baroreceptors are denervated, there is no discharge in<br />

the afferent fibers from the perfused sinus and no drop in the<br />

animal’s arterial pressure or heart rate when the perfusion<br />

pressure is below 30 mm Hg (Figure 33–6). At carotid sinus<br />

perfusion pressures <strong>of</strong> 70–110 mm Hg, there is a near linear<br />

relationship between perfusion pressure and the fall in systemic<br />

blood pressure and heart rate. At perfusion pressures<br />

above 150 mm Hg there is no further increase in response, presumably<br />

because the rate <strong>of</strong> baroreceptor discharge and the<br />

degree <strong>of</strong> inhibition <strong>of</strong> sympathetic nerve activity are maximal.<br />

From the foregoing discussion, it is apparent that the baroreceptors<br />

on the arterial side <strong>of</strong> the circulation, their afferent<br />

connections to the medullary cardiovascular areas, and the<br />

efferent pathways from these areas constitute a reflex feedback<br />

mechanism that operates to stabilize blood pressure and heart<br />

Phasic aortic<br />

pressure<br />

Mean arterial pressures (mm Hg)<br />

50<br />

75<br />

100<br />

125<br />

200<br />

0<br />

0.5<br />

1.0<br />

Time (s)<br />

FIGURE 33–5 Discharges (vertical lines) in a single afferent<br />

nerve fiber from the carotid sinus at various levels <strong>of</strong> mean<br />

arterial pressures, plotted against changes in aortic pressure with<br />

time. Baroreceptors are very sensitive to changes in pulse pressure as<br />

shown by the record <strong>of</strong> phasic aortic pressure. (Reproduced with<br />

permission from Berne RM, Levy MN: Cardiovascular <strong>Physiology</strong>, 3rd ed. Mosby, 1977.)<br />

1.5<br />

2.0<br />

% fall in systemic blood pressure<br />

80<br />

70<br />

60<br />

50<br />

40<br />

30<br />

20<br />

10<br />

0<br />

50 100 150 200<br />

Pressure in carotid sinus (mm Hg)<br />

FIGURE 33–6 Fall in systemic blood pressure produced by<br />

raising the pressure in the isolated carotid sinus to various<br />

values. Solid line: Response in a normal monkey. Dashed line: Response<br />

in a hypertensive monkey, demonstrating baroreceptor resetting<br />

(arrow).<br />

rate. Any drop in systemic arterial pressure decreases the<br />

inhibitory discharge in the buffer nerves, and there is a compensatory<br />

rise in blood pressure and cardiac output. Any rise<br />

in pressure produces dilation <strong>of</strong> the arterioles and decreases<br />

cardiac output until the blood pressure returns to its previous<br />

normal level.<br />

BARORECEPTOR RESETTING<br />

In chronic hypertension, the baroreceptor reflex mechanism<br />

is “reset” to maintain an elevated rather than a normal blood<br />

pressure. In perfusion studies on hypertensive experimental<br />

animals, raising the pressure in the isolated carotid sinus lowers<br />

the elevated systemic pressure, and decreasing the perfusion<br />

pressure raises the elevated pressure (Figure 33–6). Little<br />

is known about how and why this occurs, but resetting occurs<br />

rapidly in experimental animals. It is also rapidly reversible,<br />

both in experimental animals and in clinical situations.<br />

ROLE OF BARORECEPTORS IN SHORT-<br />

TERM CONTROL OF BLOOD PRESSURE<br />

The changes in pulse rate and blood pressure that occur in humans<br />

on standing up or lying down are due for the most part<br />

to baroreceptor reflexes. The function <strong>of</strong> the receptors can be<br />

tested by monitoring changes in heart rate as a function <strong>of</strong> increasing<br />

arterial pressure during infusion <strong>of</strong> the α-adrenergic<br />

agonist phenylephrine. A normal response is shown in Figure<br />

33–7; from a systolic pressure <strong>of</strong> about 120 to 150 mm Hg,<br />

there is a linear relation between pressure and lowering <strong>of</strong> the<br />

heart rate (greater RR interval). Baroreceptors are very important<br />

in short-term control <strong>of</strong> arterial pressure. Activation <strong>of</strong><br />

the reflex allows for rapid adjustments in blood pressure in

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