Contribution of bradykinin to the cardioprotective effects of ACE inhibitors
Contribution of bradykinin to the cardioprotective effects of ACE inhibitors
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DOI：
10.1016/s1520-765x(03)90062-9
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发表时间：
2003-01-01
影响因子：
1.6
通讯作者：
Brown, N
中科院分区：
文献类型：
--
作者：
Murphey, L;Vaughan, D;Brown, N
缓激肽通过其B-2受体刺激内皮释放许多血管扩张剂，如一氧化氮、前列环素和内皮源性超极化因子（EDHF）。血管紧张素转换酶（ACE）抑制剂通过减少其降解和增加B-2受体敏感性来增强局部缓激肽的作用。临床和实验研究表明，阻断B-2受体可减弱ACE抑制剂的抗高血压、抗肥大和抗动脉粥样硬化作用。因此，证据强烈支持缓激肽在介导ACE抑制剂的心血管益处中的作用。(C)2003年欧洲心脏病学会。
Bradykinin, through its B-2 receptor, stimulates endothelial release of a number of vasodilators, such as nitric oxide, prostacyclin, and endothelium-derived hyperpolarizing factor (EDHF). Angiotensin-converting enzyme (ACE) inhibitors enhance the effects of local bradykinin by decreasing its degradation and by increasing B-2 receptor sensitivity. Clinical and experimental studies demonstrate that blockade of the B-2 receptor attenuates the antihypertensive, antihypertrophic, and antiatherosclerotic effects of ACE inhibitors. Thus, the evidence strongly supports a role for bradykinin in mediating the cardiovascular benefits of ACE inhibitors. (C) 2003 The European Society of Cardiology.