Takata M, Sugimoto T, Matsumoto M, Iida H, Mizumura Y
J Cardiovasc Pharmacol. 1981 Nov-Dec;3(6):1260-8. doi: 10.1097/00005344-198111000-00013.
The role of bradykinin potentiation in the antihypertensive effect of captopril was assessed in conscious rabbits with two-kidney, one-clip hypertension. On the 35th day after clipping the renal artery, a bolus injection of bradykinin 0.2 microgram/kg was repeated at 15-min intervals three times before and for 180 min after the administration of captopril 0.5 mg/kg. The magnitude and duration of captopril-induced hypotension were more marked in hypertensive rabbits than in controls. The bradykinin-induced hypotension was markedly enhanced by captopril. However, the bradykinin potentiation by captopril was not correlated with its vasodepressive effect. On the other hand, a close relationship (r = 0.825, p less than 0.001) was observed between plasma renin activity and the maximum reduction in blood pressure induced by captopril. The experiment performed after sodium depletion for 7 days revealed that the bradykinin potentiating effect of captopril was not affected by sodium depletion. Therefore, it is concluded that the vasodepression by captopril does not necessarily depend on its bradykinin potentiating action and the latter is not influenced by the renin-angiotensin system or fluid volume depletion.
在两肾一夹型高血压清醒兔中评估缓激肽增强作用在卡托普利降压效应中的作用。在夹闭肾动脉后第35天，在给予0.5mg/kg卡托普利之前和之后180分钟内，每隔15分钟重复静脉注射0.2μg/kg缓激肽3次。卡托普利诱导的低血压的程度和持续时间在高血压兔中比在对照兔中更明显。卡托普利可显著增强缓激肽诱导的低血压。然而，卡托普利对缓激肽的增强作用与其血管舒张作用无关。另一方面，观察到血浆肾素活性与卡托普利诱导的最大血压降低之间存在密切关系（r = 0.825，p < 0.001）。在钠耗竭7天后进行的实验表明，卡托普利的缓激肽增强作用不受钠耗竭的影响。因此，得出结论，卡托普利的血管舒张作用不一定依赖于其缓激肽增强作用，且后者不受肾素-血管紧张素系统或体液容量耗竭的影响。
