Abnormal vascular tone and reactivity is common in essential hypertension in the easily accessible limb vessels, but little is known of their renal vascular reactivity despite the known importance of this bed. Both enhanced vasodilator responses to nonspecific vasodilators, and enhanced constrictor responses, to angiotenin II, occur in some patients with essential hypertension. One goal of this proposal is to ascertain whether the abnormality of vascular tone and responsiveness is restricted to patients in whom modulation of adrenal and renal responsiveness to angiotensin II with changes in sodium intake is normal. A second goal is to ascertain whether the renal vascular response to calcium channel blockade, induced through infusion of diltiazem into the renal artery, is enhanced in the same patients. An additional goal is to exploit a situation in which arterial and renal vein catheters are placed, to examine the influence of route of sodium chloride administration--oral, intravenous, into the renal or superior misenteric artery--on renal hormonal release and sodium excretion in normal man and in subgroups of patients with essential hypertension. Finally, studies with beta-adrenergic blockade have made it clear that renin release induced by psychological stress is mediated by a beta-adrenergic receptor, but the enhanced renal vascular response was not influenced despite blunting of the renin response, suggesting that angiotensin was not involved. Phentolamine, the alpha-adrenergic blocking agent, infused into the renal artery will be employed to identify the possible role of neurally-released norepinephrine as the mediator. Successful completion of these protocols will provide a more clear insight into the renal contribution to pathogenesis of essential hypertension, and more information on the responsible mediators.
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