Bönner G, Schunk U
Adv Exp Med Biol. 1986;198 Pt B:321-7. doi: 10.1007/978-1-4757-0154-8_40.
Bradykinin is one of the most potent vasodilators and in the kidney it develops a marked diuretic and natriuretic action. The natriuretic effect of the peptide is mediated by prostaglandins. The mechanism of bradykinin induced vasodilation, however, is not yet known. Therefore, in this study the blood pressure lowering effect of bradykinin was investigated in five normotensive volunteers. Bradykinin was injected intravenously in doses between 0.001 and 7.5 micrograms/kg of body weight. Intraarterially measured blood pressure decreased in a dose related manner from 0.25 to 1.0 micrograms/kg. Changes in oral salt intake (10 to 300 nmol Na+/d) had no effect on the action of bradykinin as well as pretreatment with either indomethacin (2 X 50 mg) or propranolol (80 mg). Captopril (25 mg) potentiated the blood pressure lowering effect of bradykinin about 20-fold. In four patients with renal hypertension bradykinin provoked a more marked reduction in arterial blood pressure, while potentiation by captopril was not different in the hypertensives if compared to the normotensives. The results of our studies show that bradykinin lowers blood pressure by a direct mechanism, which acts independently of salt intake, beta-receptors and prostaglandins. Inhibition of inactivation of bradykinin by captopril enhances its activity markedly. In renal hypertension the arterial vessels are more sensitive to bradykinin than in normotension, probably indicating a lack of endogenous kinins in these patients.
缓激肽是最有效的血管舒张剂之一，在肾脏中它具有显著的利尿和利钠作用。该肽的利钠作用由前列腺素介导。然而，缓激肽诱导血管舒张的机制尚不清楚。因此，在本研究中，对五名血压正常的志愿者进行了缓激肽降压作用的研究。以0.001至7.5微克/千克体重的剂量静脉注射缓激肽。动脉内测量的血压在剂量为0.25至1.0微克/千克时呈剂量相关下降。口服盐摄入量的变化（10至300纳摩尔钠/天）对缓激肽的作用没有影响，吲哚美辛（2×50毫克）或普萘洛尔（80毫克）预处理也无影响。卡托普利（25毫克）使缓激肽的降压作用增强约20倍。在四名肾性高血压患者中，缓激肽使动脉血压降低更为显著，而与血压正常者相比，卡托普利在高血压患者中的增效作用并无差异。我们的研究结果表明，缓激肽通过一种直接机制降低血压，该机制独立于盐摄入、β受体和前列腺素发挥作用。卡托普利抑制缓激肽的失活可显著增强其活性。在肾性高血压中，动脉血管对缓激肽比血压正常时更敏感，这可能表明这些患者体内内源性激肽缺乏。
