TY - JOUR
T1 - Evaluation of the chronotropic property of captopril in hypertensive patients
AU - Imai, Yutaka
AU - Abe, Keishi
AU - Sato, Makito
AU - Haruyama, Toshiaki
AU - Hiwatari, Masao
AU - Goto, Toshikazu
AU - Sato, Ko
AU - Kasai, Yutaka
AU - Tajima, Jiro
AU - Yoshinaga, Kaoru
N1 - Funding Information:
From the Second Department School of Medicine. This work was supported in part by a research grant from Cardiovascular Disease (54-A-2) from the Ministry of Health and Welfare, Japan. Received for publication Jan. 26. 1981; revision accepted June 2, 1981. Reprint requests: Yutaka Imai, M.D., Second Dept. of Medicine, University, l-l Seiryocho, Sendai 980, Japan.
PY - 1982/12
Y1 - 1982/12
N2 - Captopril was administered (50 mg orally) to 88 untreated hypertensive patients (70 with essential hypertension, eight with renal arterial disease, 10 with renal parenchymal disease) and to 25 hypertensive patients treated with sympatholytic or β-blocking agent (20 with essential hypertension, five with renal arterial disease). In the former group, captopril caused a decrease in heart rate (HR) in 18 patients and an increase in only two. As a whole, captopril caused significant decrease in blood pressure without increase in HR. Significant negative correlation was observed between change in HR and plasma renin activity obtained before captopril administration (n = 79, r = -0.425, p < 0.0001). Hypotensive and chronotropic effects of captopril were almost identical in untreated and treated patients. Hypotensive effects caused by captopril and nifedipine (20 mg orally) were almost identical. Nifedipine caused reflex tachycardia, while captopril caused slight bradycardia. Absence of compensatory tachycardia appears to be related to reduction of endogenous angiotensin II by captoprill.
AB - Captopril was administered (50 mg orally) to 88 untreated hypertensive patients (70 with essential hypertension, eight with renal arterial disease, 10 with renal parenchymal disease) and to 25 hypertensive patients treated with sympatholytic or β-blocking agent (20 with essential hypertension, five with renal arterial disease). In the former group, captopril caused a decrease in heart rate (HR) in 18 patients and an increase in only two. As a whole, captopril caused significant decrease in blood pressure without increase in HR. Significant negative correlation was observed between change in HR and plasma renin activity obtained before captopril administration (n = 79, r = -0.425, p < 0.0001). Hypotensive and chronotropic effects of captopril were almost identical in untreated and treated patients. Hypotensive effects caused by captopril and nifedipine (20 mg orally) were almost identical. Nifedipine caused reflex tachycardia, while captopril caused slight bradycardia. Absence of compensatory tachycardia appears to be related to reduction of endogenous angiotensin II by captoprill.
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U2 - 10.1016/0002-8703(82)90165-X
DO - 10.1016/0002-8703(82)90165-X
M3 - Article
C2 - 6128916
AN - SCOPUS:0020445682
VL - 104
SP - 1339
EP - 1345
JO - American Heart Journal
JF - American Heart Journal
SN - 0002-8703
IS - 6
ER -