Acute and chronic effect of captropril in hypertensive patients.

Acute and chronic antihypertenslve effects of the angiotensin conferring enzyme inhibitor, captoprii (SQ 14,225), was assessed in 29 consecutirely-studled patients with hypertension. (Mean arterial pressure, 110-160 mm Hg). Eighteen patients had essential hypertension (three with high plasma renln activity (PRA), 11 with normal PRA, four with low PRA); eight had renovascular hypertension (four with high PRA and four with normal PRA); two had end-stage renal parenchyma! disease, and one had primary aldosteronism due to bilateral adrenal hyperplasia. Antihypertensive drugs were discontinued approximately 1 month prior to being studied. Patients were studied on the metabolic unit and received a constant 100 mEq sodium and 60 mEq potassium/day diet Control data were obtained for 3 days with placebo treatment Captoprii was then begun at 10 or 25 mg and increased to a maximum of 100 or 150 mg four times per day. During die first 3-10 days of treatment, 16 patients (55%) achieved normal blood pressure (BP) on captoprii alone, and six patients (21%) achieved it with the addition of a diuretic Six patients (21%) exhibited a fall In diastoiic blood pressure (DBP) greater than 10 mm Hg, but did reach normal. Captoprii was ineffective in lowering BP in one patient (low PRA, essential hypertension). Of the 22 patients who achieved normal BP, all but one (normal PRA) exhibited a rise in PRA, and all exhibited a fall in plasma aldosterone concentration (PAC). Blood pressure, PRA, and PAC responses were independent of either etiologic classification or renln subtype. The mean effective daily dose of captoprii was 261 mg. Nineteen patients were followed from 1-18 months on maintenance captoprii therapy. Blood pressure remained well controlled, without evidence of toxldty, in all patients, although medication adjustment (either a dose increase or a diuretic) was required in all but five patients by the fifth outpatient month. The PRA remained elevated in 12 patients up to 6 months after discharge. The BP response was not predicted by control PRA, PAC, or BP, although there was a correlation between acute renin rise and BP reduction. These results indicate that captoprii is an effective, well-tolerated agent for the longterm treatment of hypertension of multiple etiologies. These results are consistent with captopril's known ability to block angiotensin II formation and perhaps to prevent bradyklnin degradation, although the primary mechanism responsible for BP reduction remains to be elucidated. (Hypertension 2: 567-575, 1980)