Imai Y, Abe K, Yoshinaga K
Tohoku J Exp Med. 1981 Feb;133(2):243-4. doi: 10.1620/tjem.133.243.
Captopril, an orally active converting enzyme inhibitor, was administered in a dose of 50 mg 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 less than 0.001).
卡托普利是一种口服有效的血管紧张素转换酶抑制剂，对88例未经治疗的高血压患者（70例原发性高血压患者、8例肾动脉疾病患者、10例肾实质疾病患者）给予50毫克的剂量。卡托普利使18例患者心率降低，但使2例患者心率升高。其余68例患者心率未发生变化。总体而言，卡托普利使血压显著降低，且心率没有代偿性增加。肾动脉疾病患者中卡托普利引起的心率变化显著高于原发性高血压患者。在服用卡托普利前即刻测得的心率变化与血浆肾素活性之间观察到显著的负相关（n = 79，r = 0.425，p＜0.001）。
