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Hemodynamic and volume changes associated with captopril.
Author(s) -
Robert C. Tarazi,
E L Bravo,
F. M. Fouad,
Per Omvik,
Robert Cody
Publication year - 1980
Publication title -
hypertension
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.986
H-Index - 265
eISSN - 1524-4563
pISSN - 0194-911X
DOI - 10.1161/01.hyp.2.4.576
Subject(s) - captopril , medicine , blood pressure , hemodynamics , trandolapril , cardiology , angiotensin converting enzyme , ace inhibitor
SUMMARY The effects of captopril on bemodynamic, rolmne, and neurohumoral indices were inrestigated in 33 patients with essential hypertension or renal arterial disease. Changes associated with treatment were studied under two conditions: immediately (V4 to 1 boar) after administration of the drug, or after 5 to 7 days of therapy. Blood pressure (BP) reduction in both conditions was due to a reduction in total peripheral resistance (TPR) (r = 0.714, p < 0.001 for A MAP / TPR); there was no significant change in either cardiac output or heart rate. The immediate BP and TPR responses were significantly related to pretreatment plasma renin activity (PRA) (r = 0.737, p < 0.001), but this correlation was much weaker (r - 0392, p > 0.50) after maintained treatment. Response to therapy could not be predicted from either bemodynamic or volume characteristics of the patients (r - 0.265, NS for A MAP / TBV and -0.262, NS for A MAP / cardiac output). There was no significant change in body weight during treatment, while plasma volume Increased slightly (+7% ± 2.8 SE, p < 0.05) but only in those patients who maintained a good BP response to captopril. Simultaneously, plasma aldosterone (PA) levels were reduced in relation to pretreatment level (r = 0.955, p < 0.001). Thus, whereas the hemodynamic pattern of response to captopril remained unchanged during therapy, its relationship to pretreatment PRA became progressively weaker. The clinical antihypertensive effectiveness of captopril was therefore not related to either humoral, hemodynamic, or volume characteristics of this group of patients. The unusual pattern of lack of significant plasma volume expansion during therapy might be related in part to sustained reduction of plasma aldosterone levels.

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