INFLUENCE OF PULSATILE PRESSURE ON THE BAROREFLEX

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An increased mean arterial pressure increases baroreceptor activity which reflexly inhibits sympathetic activity and buffers the rise in pressure. In vivo, the baroreceptors are exposed to a pulsatile pressure that may modify the baroreflex by altering the amount of baroreceptor activity per unit time, the pattern of activity, and/or the rate of adaptation of the reflex during sustained baroreceptor stimulation. The magnitude and selectively of sympathetic inhibition may not only be a function of the amount of baroreceptor activity per unit time but may be a function of the phasic pattern of activity. The first specific aim is to determine and contrast the effects of static and pulsatile activation of baroreceptors on the baroreflex for the same level of baroreceptor activity. The second aim is to determine the relative influence of baroreceptor activity/unit time, number of bursts of activity/unit time, activity/burst, and peak instantaneous activity on the baroreflex. The third aim is to determine the effect of the pattern of baroreceptor activation on the regional selectivity of the reflex. The magnitude and selectivity of "adaptation", i.e. the escape of sympathetic activity from baroreflex inhibition during a sustained increase in pressure, may be dependent on the pattern of stimulation and thus altered during pulsatile pressure. The fourth aim is to characterize and examine the mechanism responsible for the adaptation of baroreceptors during static and pulsatile pressure. The fifth aim is to determine the role of "central adaptation" during static and pulsatile pressure in normotensive and hypertensive animals. To achieve these goals the isolated carotid sinuses in anesthetized dogs will be exposed to controlled levels of static and pulsatile pressure while carotid sinus diameter, baroreceptor activity, and efferent sympathetic activity are measured. Simultaneous recordings of afferent and efferent activity and simultaneous recordings of two efferent activities will enable the role of the pattern of baroreceptor activity and the regional selectivity of the responses to be evaluated. Electrical stimulation of afferent fibers will also be performed to examine central effects of pulsatility. The results should define the functional significance of the phasicity of baroreceptor activity and its role in adjusting autonomic control in a specific and selective way. The results may have important implications pertaining to circulatory disorders such as hypertension.