Constrasts and similarities of acute hemodynamic responses to specific antagonism of angiotensin II ([Sar1, Thr8] A II) and to inhibition of converting enzyme (captopril).

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Abstract
The early blood pressure and hemodynamic effects of the converting enzyme inhibitor (CEI), captopril, were compared in 23 hypertensive patients with those of a specific angiotensin II [AII] antagonist (AA), [Sar1, Thr8] A II. AA reduced mean arterial pressure (MAP) > 10 mm Hg only in 7 of 23 patients vs. 15 of 23 who responded to CEI (P < 0.02). With both drugs, changes in MAP were not associated with significant changes in cardiac output (P > 0.10 for both drugs), but correlated with changes in systemic resistance (TPR); r [correlation coefficient] = 0.84, P < 0.001 for AA and r = 0.71, P < 0.001 for CEI. Changes in TPR and MAP correlated significantly and inversely with log plasma renin activity in both instances; for AA, r = - 0.829 and for CEI, r = -0.737; P < 0.001 for both. The slopes of the 2 regression lines were not significantly different, but the intercepts were +8.47 mm Hg for AA vs. -10.17 mm Hg for CEI (P < 0.001). This quantitative difference in response could be attributed to an agonistic effect of [Sar1, Thr8] A II or to an additional vasodilator effect of captopril.