This research will mechanistically describe a poorly understood aspect of arterial baroreflex control which can impact the regulation of systemic arterial pressure. The arterial pressure - heart period relation does not simply describe a sigmoid, but demonstrates a hysteresis. That is, heart period responses depend on the direction of pressure change; at any pressure, heart rates are slower during falls than during rises. This characteristic of the arterial baro-reflex may have significant clinical import especially in understanding hypotensive syndromes. This work will examine the likely key component of baroreflex hysteresis -- barosensory vessel distensibility. Lesser distensibility may not only alter baroreflex sensitivity, but also augment baroreflex hysteresis. If hysteresis is exaggerated by arterial stiffening, this alone could produce discordant heart rate responses to hypotensive stimuli, leading to reduced cerebral blood flow and syncope. Rapid pharmacologically induced arterial pressure changes will be used to characterize autonomic baroreflex hysteresis through the full reflex range. The autonomic responses and pressure changes will be related to concurrent measures of carotid barosensory vessel stretch to examine the viscoelastic component of baroreflex hysteresis. Since the prevailing stretch determines barosensory vessel distensibility, hysteresis will be characterized under two conditions to vary the level of stretch (supine and 45 tilt). Since individuals with greater carotid stiffness may demonstrate a maladaptive exaggerated hysteresis, these relationships will be examined not only in normotensives but also in middle aged hypertensives who have been shown previously to have greater carotid stiffness. This work may provide key insight to understand the high prevalence of arterial pressure dysregulation in order and hypertensive individuals.
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