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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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

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 antagonist (AA), [ Sar1, Thr8] A II. AA reduced mean arterial pressure (MAP) greater than 10 mm Hg only in seven of 23 patients vs 15 of 23 who responded to CEI (p less than 0.02). With both drugs, changes in MAP were not associated with significant changes in cardiac output (p greater than 0.10 for both drugs), but correlated with changes in systemic resistance ( TPR); r = 0.84, p less than 0.001 for AA and r = 0.71, p less than 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 less than 0.001 for both. The slopes of the two regression lines were not significantly different but the intercepts were +8.47 mm Hg for AA vs -10.17 mm Hg for CEI (p less than 0.001). This quantitative difference in response could be attributed either to an agonistic effect of [ Sar1, Thr8] A II or to an additional vasodilator effect of captopril.[1]


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