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

SUMMARYHemodynamic responses to a new angiotensin II antagonist, [Sarl, Thr8]A II, were studied in 17 hypertensive patients whose plasma renin activity (PRA) ranged from 0.2–42.0 ng/ml/hr. With infusion of 1.0 μg/kg/min, mean arterial pressure (MAP) rose 10 mm Hg in six patients, was unchanged in six patients, and decreased 2 10 mm Hg in five patients. There was no significant change in either cardiac index or heart rate in any of these groups, so variations in MAP were related only to corresponding change in total peripheral resistance (△TPR) (r = 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. These results contrast with the depression in cardiac output reported to occur with saralasin in compensated hypertensive patients regardless of blood pressure response to that drug. Such differences in hemodynamic response between two angiotensin antagonists imply that conclusions regarding cardiovascular role of A II cannot be inferred from results with one antagonist alone. Further, because of the absence of cardiac output depression, [Sarl, Thr8]A II might be safe for patients with cardiac disease.