We have demonstrated a) that cardiopulmonary mechaoreceptos (CPR) play an important role in reflex regulation of renin release in humans, b) that some patients with lowrenin hypertension have a large cardiopulmonary blood volume and low renin values, c) that in hypertension there is a negative correlation between the left atrial diameter (by echo) and renin levels. These obervations form the basis for the hypothesis that in human hypertension the abnormal renin distribution (high-low) may in part be caused by an abnormal blood volume distribution from the peripheral to cardiopulmonary capacitance space, which causes an abnormal stretch of cardiopulmonary receptors and these receptors in turn alter the reflex release of renin. We want to 1) define the subset of patients in whom the renin abnormalities are clearly related to abnormalities in blood volume disbribution, 2) to investigate the mechanism responsible for the abnormal volume distribution in hypertension. Two specific protocols to achieve these objectives are outlined. In one we will induce acute volume shifts in patients and controls and determine whether levels renin, norepinephrine and vasopressin can be altered towards normal values. In the second protocol, the nature of the venous dysfunction and its relationship to contractile and responsivity characteristics of arterioles will be investigated. In this protocol we will assess the vascular and nonvascular responses to sympathetic agonists and antagonists. Responses to nonsympathetic vasoactive compounds will also be studied. All protocols include a carefully matched normotensive control group.
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