The Effect of Captopril on Heart Rate in Several Types of Hypertensive Patients

Abstract

I, Y., ABE, K. and YOSHINAGA, K. The Effect of Captopril on Heart Rate in Several Types of Hypertensive Patients. Tohoku J. exp. Med., 1981, 133 (2), 243-244-Captopril, an orally active converting enzyme inhibitor, was administered in a dose of 50mg to 88 untreated hypertensives (70 essential hypertensives, 8 patients with renal arterial disease, 10 patients with renal parenchymal disease). Captopril caused a decrease in heart rate in 18 patients, but an increase in 2 patients. In the remaining 68, heart rate did not change. As a whole, captopril caused a significant decrease in blood pressure without compensatory increase in heart rate. The change in heart rate caused by captopril in patients with renal arterial disease was significantly higher than that in essential hypertensives. A significant negative correlation was observed between the change in heart rate and plasma renin activity obtained immediately before captopril administration (n=79, r=-0.425, p<0.001).-captopril; heart rate; blood pressure; plasma renin activity Captopril has a potent antihypertensive action and, hemodynamically, behaves like a vasodilator (Cody et al. 1978). Several vasodilators have been shown to increase heart rate. Reflex tachycardia is one of undesirable effects of vasodilators when used for the treatment of hypertension. In this study we examined the effect of captopril on blood pressure and heart rate in several types of hypertensive patients. Studies were performed on 88 untreated hypertensives (70 essential hypertensives, 8 patients with renal arterial disease and 10 patients with renal parenchymal disease). The diagnosis of renal arterial lesion was made angiographically, while that of renal parenchymal disease was made by renal biopsy. The study was started on fasted patients between 9:00 and 9:30 a.m. The subjects were kept in supine position during the study period. After at least 30min of pre-control period, blood pressure and heart rate were measured every 10min for 1hr. The terms used for 30min, 20min, 10min before and immediately before drug administration were expressed as -30min, -20min, -10min and 0 time, respectively. At the end of this control period, blood was collected for the measurement of control plasma renin activity (PRA), after which 50mg of captopril was administered orally. Blood pressure and heart rate were measured every 30min with an arteriosonde (Roche) or a mercury sphygmomanometer and a cardiotachometer or palpation of radial pulse. Since the spontaneous change in heart rate measured in each patient during the control period (0, -10, -20, -30min) was 1.7±1.6 beats/min (mean±S.D.), the change in heart rate above ±4.9 beats/min [±(mean+2S.D.)] after drug administration was judged as a significant one. PRA was measured using radioimmunoassay of angiotesin I. Results are expressed as mean±S.D. Statistical analysis of the data was performed according to Student's t test.