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Converting enzyme inhibition with captopril in patients with primary hyperaldosteronism
Author(s) -
Luderer John R,
Demers Laurence M,
Harrison Timothy S,
Hayes Arthur H
Publication year - 1982
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1038/clpt.1982.38
Subject(s) - captopril , aldosterone , hyperaldosteronism , renovascular hypertension , plasma renin activity , endocrinology , blood pressure , medicine , angiotensin converting enzyme , essential hypertension , enalapril , pharmacology , hemodynamics , renin–angiotensin system , chemistry
The humoral and hemodynamic effects of converting enzyme inhibition with captopril are presented in two 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 (±SEM) plasma renin activity (PRA) rose from 5.0 ± 1.4 to 35.3 ± 5.3 ng/ml/hr (P < 0.001) and mean (±SEM) plasma aldosterone (PA) declined from 25.8 ± 2.9 to 15.1 ± 1.9 ng/ml (P < 0.01) after captopril. In two 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 responsed appropriately to captopril. These cases illustrate that a disease process can modify the response to a drug and demonstrate that, in patients with PHA, captopril does not stimulate PRA, induces only minor decrements in PA, and is relatively ineffective as an antihypertensive. Clinical Pharmacology and Therapeutics (1982) 31, 305–311; doi: 10.1038/clpt.1982.38