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Kinins as therapeutic agents in cardiovascular and renal diseases.

机译:激肽作为心血管和肾脏疾病的治疗剂。

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摘要

A fair amount of data indicates that bradykinin and lysyl-bradykinin exert arterial, cardiac and renal effects which afford protection against organ damage in diseases, especially in the settings of ischemia or diabetes. The concept of kinins acting as therapeutic agents is supported by the wide use of angiotensin I-converting enzyme (ACE) inhibitors. These inhibitors indeed potentiate kinin action by inhibiting kinin degradation. Experimental evidence strongly suggests that the cardiac and renal effects of ACE inhibitors are due, at least in part, to kinins. Angiotensin AT1 receptor antagonists act also partly through kinins. This paper reviews available evidence supporting a role for kinins in the therapeutic effect of current drugs. It then discusses the opportunity to develop new drugs based on kinin action. Direct activation of the kinin B2 receptor by pharmacological agonists might provide higher therapeutic benefit than existing kinin- potentiating drugs. Possible occurrence of side effects is however a concern.
机译:大量数据表明,缓激肽和赖氨酰缓激肽具有动脉,心脏和肾脏的作用,从而可以抵抗疾病中的器官损害,尤其是在缺血或糖尿病的情况下。激肽作为治疗剂的概念得到了血管紧张素I转换酶(ACE)抑制剂的广泛使用的支持。这些抑制剂确实通过抑制激肽降解而增强了激肽作用。实验证据强烈表明,ACE抑制剂的心脏和肾脏作用至少部分归因于激肽。血管紧张素AT1受体拮抗剂也部分通过激肽起作用。本文综述了现有证据支持激肽在当前药物的治疗作用中的作用。然后讨论了基于激肽作用开发新药的机会。与现有的激肽增强药相比,药理激动剂直接激活激肽B2受体可能提供更高的治疗益处。但是,可能会出现副作用。

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