Cardiovascular, renal, and endocrine response to atrial natriuretic peptide in angiotensin II mediated hypertension. Circ. Res

Studies done in vitro have demonstrated that atrial natriuretic peptide (ANP) antagonizes angiotensin H-mediated contraction of vascular smooth muscle. The present studies were designed to examine the in vivo actions of ANP in acute angiotensin II-mediated hypertension. The cardiovascular, renal, and hormonal effects of intravenous ANP were evaluated in anesthetized nor mo tensive (n = 6) and hyper-tensive (n = 6) dogs. In both groups, ANP (3.0 /u.g/kg bolus, 0.3 jug/kg/min continuous infusion) reduced arterial pressure and cardiac output without changing systemic vascular resistance. ANP specifically reduced renal vascular resistance and increased sodium excretion. The natriuresis ob-served was greater in hypertensive than in normotensive dogs. This occurred without a significant change in glomerular filtration rate or aldosterone. The ANP-mediated reduction in arterial pressure was associated with an increase in circulating arginine vasopressin and catecholamines but not in renin. These studies demonstrate that (1) ANP-mediated hypotension results from a reduction in cardiac output without changing systemic vascular resistance, (2) ANP acts as a specific renal vasodi-lator, (3) ANP-mediated natriuresis can occur without alteration in glomerular filtration rate or aldosterone, and (4) ANP specifically inhibits the release of renin without inhibiting the release of other circulating vasoconstrictors. (Circulation Research 1986;59:663-667