Bönner G, Schunk U, Kaufmann W
Cardiology. 1985;72 Suppl 1:190-3. doi: 10.1159/000173973.
To investigate the cardiovascular effects of bradykinin (BK), the peptide was injected into 6 normotensive volunteers in the supine position. BK was given intravenously as a bolus in a dose of 0.001-7.5 microgram BK/kg body weight. Intraarterial blood pressure decreased dose related in a range of 0.25-1.0 microgram BK/kg body weight. Pretreatment with 2 X 50 mg indomethacin or 80 mg propranolol as well as changes in oral salt intake (from 10 to 300 mmol Na+/day) had no effect on the blood pressure-lowering effect of BK. Captopril (25 mg) potentiated the effect of BK 20- to 50-fold. In primary hyperaldosteronism, renal kallikrein activity and absolute vascular reaction to BK was increased. The results showed clearly that in man, similarly as in rats, BK lowers blood pressure by direct vasodilation and acts independently of prostaglandins, beta-receptors or salt intake.
为研究缓激肽（BK）对心血管系统的影响，将该肽注入6名仰卧位的血压正常志愿者体内。BK以静脉推注的方式给药，剂量为0.001 - 7.5微克BK/千克体重。动脉血压在0.25 - 1.0微克BK/千克体重范围内呈剂量依赖性下降。用2×50毫克吲哚美辛或80毫克普萘洛尔预处理以及口服盐摄入量的变化（从10至300毫摩尔钠/天）对BK的降压作用均无影响。卡托普利（25毫克）使BK的作用增强了20至50倍。在原发性醛固酮增多症中，肾激肽释放酶活性和对BK的绝对血管反应增加。结果清楚地表明，在人类中，与在大鼠中一样，BK通过直接血管舒张降低血压，且其作用独立于前列腺素、β受体或盐摄入量。
