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Cardiac and hormonal effects of enalapril in hypertension
Insights
Enalapril effectively lowers blood pressure in hypertensive men. Cardiac performance remained unchanged, possibly due to enalapril inhibiting norepinephrine release during exercise.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Hypertension management requires understanding drug effects on cardiac performance.
- Enalapril is an angiotensin-converting enzyme inhibitor used for hypertension.
Purpose of the Study:
- To evaluate the effects of enalapril on cardiac performance in hypertensive men.
- To assess changes in plasma renin activity (PRA) and norepinephrine (NE) during exercise.
Main Methods:
- Systolic time measurements, echocardiography, and bicycle exercise testing were employed.
- Cardiac output, stroke volume, PRA, and NE were measured at rest and during exercise.
- 16 male hypertensives were treated with enalapril (N=11) or placebo (N=5) for 12 weeks.
Main Results:
- Enalapril significantly reduced mean arterial pressure.
- Cardiac performance metrics (e.g., ejection time, fractional shortening) remained unchanged at rest and during exercise.
- Enalapril induced a compensatory rise in PRA and attenuated the exercise-induced rise in plasma NE concentration.
Conclusions:
- Enalapril effectively lowers blood pressure without altering cardiac performance in hypertensive individuals.
- The observed effects may be linked to enalapril's inhibition of angiotensin II-mediated norepinephrine release.
Abstract:
Systolic time measurements, echocardiography, and bicycle exercise testing with cardiac output determinations (CO2 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.