Bradykinin and cardioprotection: don't set your heart on it.
Bradykinin and cardioprotection: don't set your heart on it.
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缓激肽和心脏保护：不要太在意它。
DOI：
10.1006/phrs.1997.0182
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发表时间：
1997
影响因子：
9.3
通讯作者：
Levi,R
中科院分区：
文献类型：
--
作者：
Hatta,E;Rubin,LE;Seyedi,N;Levi,R
血管紧张素转换酶抑制剂被认为是保护心肌缺血和心力衰竭1，2。由于在这些情况下，肾素-血管紧张素系统被激活3，因此预防血管紧张素的产生可以很容易地解释ACE抑制剂的有益作用。然而，由于ACE抑制剂也延长了缓激肽的半衰期，并且它们的一些血管效应被缓激肽B受体2 wx拮抗剂阻断4，5，因此较高的局部激肽浓度和相关的血管舒张效应wx的相关性受到了广泛关注4，6。令人惊讶的是，缓激肽的其他重要作用，如促进外周交感神经传递wx 79和促进心脏去甲肾上腺素wx释放912，尚未得到充分强调。我们将在这里简要回顾我们的经验与缓激肽的心脏保护作用13，并讨论我们的初步证据上的看似有害的行动缓激肽在心肌缺血14，15。
ACE inhibitors are viewed as protective in myocarwx dial ischaemia and cardiac failure 1, 2. In so much as the reninangiotensin system is activated in these wx conditions 3, prevention of angiotensin production could easily explain the beneficial effects of ACE inhibitors. However, because ACE inhibitors also prolong bradykinin’s half-life and some of their vascular effects are blocked by bradykinin B-receptor2 wx antagonists 4, 5, the relevance of higher local kinin concentrations and associated vasodilating effects wx has received much attention 4, 6. Surprisingly, other important effects of bradykinin, such as the facilitation of peripheral sympathetic neurotransmission wx 79 and the promotion of cardiac norepinephrine w x release 912, have not been adequately emphasized. We will brieffy review here our experience wx with the cardioprotective effects of bradykinin 13 and discuss our preliminary evidence on the seemingly deleterious actions of bradykinin in myocardial w x ischaemia 14, 15.