Key result
Captopril is linked to a ~7-fold PRA increase in essential hypertension but not primary hyperaldosteronism.
Why the study?
Does captopril alter plasma renin activity, plasma aldosterone, and blood pressure in patients with primary hyperaldosteronism compared to those with essential or renovascular hypertension?
Population
20 patients with resistant hypertension
Comparison
Captopril vs Pre-treatment baseline
Design
Case_series
Authors
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Captopril may fail to stimulate renin in primary hyperaldosteronism; leaves open diagnostic utility in resistant hypertension pending prospective validation.
Observational (n=20)
Does captopril alter plasma renin activity, plasma aldosterone, and blood pressure in patients with primary hyperaldosteronism compared to those with essential or renovascular hypertension?
p-value: p=<0.01
Captopril is relatively ineffective as an antihypertensive and fails to stimulate plasma renin activity in patients with primary hyperaldosteronism, demonstrating that the underlying disease process modifies the pharmacological response.
Luderer et al. (1982) conducted an observational in Resistant hypertension and primary hyperaldosteronism (n=20). Captopril was evaluated on Plasma renin activity (PRA) and plasma aldosterone (PA) (p=<0.01). Captopril increased plasma renin activity from 5.0 to 35.3 ng/ml/hr (P<0.01) in 18 patients with essential hypertension, but failed to stimulate it in 2 patients with primary hyperaldosteronism.
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