The vasodilating effect of atrial natriuretic peptide in normotensive and hypertensive humans

Atrial natriuretic peptide (ANP) infused intra-arterially into the forearm results in a dose-dependent vasodilator response of rapid onset. The maximal forearm vasodilator response to ANP amounts to about 60% of the maximal forearm vasodilator response to sodium nitroprusside and combined infusion of ANP and sodium nitroprusside has an additive vasodilator effect. ANP-induced vasodilation is greater than that of postjunctional alpha 1- or alpha 2-adrenoceptor blockade or of beta 2-adrenoceptor stimulation but is smaller than due to calcium entry blockade. ANP-induced vasodilation can easily be overcome by norepinephrine and to a lesser extent by angiotension II (Ang II). The similarity of the dose-response relationships for vasodilation and for natriuresis suggests that ANP may be equally effective on its renal and vascular targets. In patients with essential hypertension, intra-arterial infusion of ANP produced a greater vasodilator response than in normotensives and this was inversely related to plasma renin activity, suggesting greater vasodilator responsiveness to ANP in low-renin hypertension. ANP caused vasodilation in humans but this may become less apparent when ANP is infused into the systemic circulation because of cardiovascular sympathetic reflex mechanisms blunting ANP vasodilation. Although the role of ANP in circulatory disease states is unclear, it appears that it could serve a physiological function as an endogenous vasodilator (and natriuretic) principle for volume homeostasis in humans.