Hemodynamics of a new angiotensin antagonist, [Sar1, Thr8]A II, in hypertensive man.

Abstract

Hemodynamic responses to a new angiotensin II [A II] antagonist, [Sar1, Thr8]A II, were studied in 17 hypertensive patients whose plasma renin activity (PRA) ranged from 0.2-42.0 ng/ml per h. With infusion of 1.0 .mu.g/kg per min, mean arterial pressure (MAP) rose .gtoreq. 10 mm Hg in 6 patients, was unchanged in 6 patients, and decreased .gtoreq. 10 mm Hg in 5 patients. There was no significant change in cardiac index or heart rate in any of these groups, so variations in MAP were related only to corresponding change in total peripheral resistance (.DELTA.TRP) (r [correlation coefficient] = 0.913, P < 0.001). The response of both MAP and TPR to the antagonist correlated closely with control PRA (r = -0.812 and -0.889, respectively, P < 0.001 for both). Stability of both cardiac index and pulmonary wedge pressure suggested that [Sar1, Thr8]A II did not alter cardiac performance. Saralasin in compensated hypertensive patients regardless of blood pressure response to that drug causes a depression in cardiac output. Apparently the cardiovascular role of A II cannot be inferred from results with 1 antagonist alone. Due to the absence of cardiac output depression, [Sar1, Thr8]A II might be safe for patients with cardiac disease.