血管紧张素II和缓激素在心脏和血管中的作用

D. Moura, H. Pinheiro, M. Q. Paiva, S. Guimaraes
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引用次数: 13

摘要

1血管紧张素和缓激素促进交感神经末梢去甲肾上腺素的释放,引起大鼠离体心房和心室正性肌力变。缓激肽的作用可通过ACE抑制剂雷米普利特增强。2缓激肽促进去甲肾上腺素在大鼠心室的释放被β2受体拮抗剂HOE-140阻断。这种反应也可以通过去除心内膜而减轻,提示从心内膜释放一种介质。血管紧张素II和缓激素促进的去甲肾上腺素释放被血管紧张素受体拮抗剂saralasin同样程度地阻断。相反,氯沙坦在一系列血管和心脏组织中只引起轻微的阻滞。这表明血管紧张素和缓激素通过与不同于已建立的AT1亚型的结前受体相互作用来发挥这些反应。这些结果表明,缓激素通过局部释放血管紧张素到非典型AT1受体介导去甲肾上腺素的释放。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Prejunctional effects of angiotensin II and bradykinin in the heart and blood vessels

1 Angiotensin and bradykinin facilitate the release of noradrenaline from sympathetic nerve terminals and cause positive inotropy in rat isolated atria and ventricles. The effect of bradykinin was enhanced by the ACE inhibitor, ramiprilat.

2 The facilitated release of noradrenaline in rat ventricle by bradykinin was blocked by the β2-receptor antagonist HOE-140. This response is also reduced by removing the endocardium, suggesting the release of a mediator from the endocardium.

3 The facilitated noradrenaline release by angiotensin II and bradykinin was blocked by the angiotensin receptor antagonist saralasin to the same extent. In contrast, losartan caused only minor blockade in a range of vascular and cardiac tissues. This suggests that angiotensin and bradykinin exert these responses by interacting with a prejunctional receptor different from the established AT1 subtype.

4 These results suggest that bradykinin mediates facilitation of noradrenaline release via the local release of angiotensin onto an atypical AT1 receptor.

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