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Cardiac and hormonal effects of enalapril in hypertension
Author(s) -
Morioka Shigefumi,
Simon Geza,
Cohn Jay N
Publication year - 1983
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.1983.219
Subject(s) - enalapril , plasma renin activity , medicine , blood pressure , cardiac output , placebo , stroke volume , enalapril maleate , heart rate , cardiology , essential hypertension , endocrinology , anesthesia , renin–angiotensin system , angiotensin converting enzyme , alternative medicine , pathology
Systolic time measurements, echocardiography, and bicycle exercise testing with cardiac output determinations (CO 2 rebreathing) were used to evaluate cardiac performance in 16 male hypertensives at the end of a 4‐wk placebo period and after 12 wk of treatment with increasing doses (maximum = 40 mg/day) of enalapril maleate (N = 11) and of placebo (N = 5). The effect of exercise on plasma renin activity (PRA) and plasma norepinephrine (NE) concentration was also measured. Mean arterial pressure was reduced by 10 mm Hg or more in all but one subject who received enalapril. In both the enalapril‐ and placebo‐treated subjects, the preejection period/left ventricular ejection time ratio and fractional shortening of the left ventricle at rest and cardiac output and stroke volume during moderate exercise did not change during the study. Enalapril induced a compensatory rise in PRA (N = 10). Compared to plasma NE concentration. 1124 ± 380 pg/ml (mean ± SD), during exercise at the end of the initial placebo period, there was attenuation of the rise of plasma NE concentration, 851 ± 290, at the same load of exercise during enalapril therapy. Unchanged cardiac performance despite effective long‐term lowering of blood pressure with enalapril may relate to inhibition of angiotensin II‐mediated facilitation of NE release from peripheral nerve endings. Clinical Pharmacology and Therapeutics (1983) 34, 583–589; doi: 10.1038/clpt.1983.219