Converting enzyme inhibition with captopril in patients with primary hyperaldosteronism

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Abstract
The humoral and hemodynamic effects of converting enzyme inhibition with captopril are presented in 2 patients with primary hyperaldosteronism (PHA). In all, 20 patients with resistant hypertension were treated with the angiotensin converting enzyme inhibitor captopril. In 18 patients with essential or renovascular hypertension mean plasma renin activity (PRA) rose from 5.0 .+-. 1.4 to 35.3 .+-. 5.3 ng/ml per h (P < 0.001), and mean plasma aldosterone (PA) declined from 25.8 .+-. 2.9 to 15.1 .+-. 1.9 ng/ml (P < 0.01) after captopril. In 2 patients with PHA the PRA was not stimulated by converting enzyme inhibition, although there was modest decline in PA and a temporary reduction in blood pressure. After surgical removal of aldosterone-producing adenomas, PRA responded appropriately to captopril. Evidently, a disease process can modify the response to a drug. Apparently in patients with PHA, captopril does not stimulate PRA, induces only minor decrements in PA and is relatively ineffective as an antihypertensive.

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