[Mechanisms of the hypotensive action of captopril in essential hypertension].
Captopril effects were studied in 27 patients with second-stage essential hypertension following administration of a single 25 mg oral dose of the drug. Blood pressure (BP), blood angiotensin-1-converting enzyme (ACE) activity, active (APR) and inactive (IPR) plasma renin levels were measured every 30 minutes for 3 hours. Before and near the end of the acute test, urinary kallikrein and catecholamine excretions were measured, and systemic and regional hemodynamic changes assessed. BP decreased in 21 patients: 11 of those had low basal APR (group 1), and 10 had normal or moderately elevated APR (group 2). The greatest hypotensive effect was observed within 1.5 hours after the administration, coinciding with the most marked ACE inhibition. There was no significant intergroup difference with respect to the extent of the hypotensive effect. No correlation was found between the hypotensive effect and the degree of ACE inhibition. All patients showed significantly decreased arteriolar tone, increased venous distensibility, decreased total peripheral resistance, and expanded end diastolic volume, while their cardiac output and heart rate remained unaffected. Hypertensive patients with low APR gave no evidence of renin-angiotensin inhibition or kallikrein-kinin activation that might have accounted for the hemodynamic effect of captopril.
D000328:Adult; D000450:Aldosterone / Q000097:blood; D002216:Captopril / Q000494:pharmacology / Q000627:therapeutic use*; D004837:Epinephrine / Q000652:urine; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D006973:Hypertension / Q000188:drug therapy*; D007610:Kallikreins / Q000652:urine; D008875:Middle Aged; D009638:Norepinephrine / Q000652:urine; D007703:Peptidyl-Dipeptidase A / Q000097:blood; D012083:Renin / Q000097:blood
D000450:Aldosterone; D002216:Captopril; D007703:Peptidyl-Dipeptidase A; D007610:Kallikreins; D012083:Renin; D009638:Norepinephrine; D004837:Epinephrine
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