期刊
BASIC & CLINICAL PHARMACOLOGY & TOXICOLOGY
卷 100, 期 6, 页码 361-365出版社
BLACKWELL PUBLISHING
DOI: 10.1111/j.1742-7843.2007.00057.x
关键词
-
Various mechanisms have been postulated to be involved in angiotensin-(1-7)-induced endothelium-dependent vasodilation. Here, we characterized the vasodilator action of angiotensin-(1-7) in the isolated guinea pig heart. Angiotensin-(1-7) (1-10 nmol, bolus) induced dose-dependent increase in the coronary flow. The coronary vasodilation induced by angiotensin-(1-7) was significantly reduced by the nitric oxide synthase inhibitor, L-N-G-nitroarginine methyl ester (L-NAME) (100 mu M) and abolished by a B-2 receptor antagonist, icatibant (100 nM). Coronary vasodilation induced by bradykinin (3 pmol, bolus) was inhibited by L-NAME and icatibant to similar extent as that induced by angiotensin-(1-7). Neither the selective AT(2) angiotensin receptor antagonist, PD123319 (1 mu M), nor the antagonist of a putative angiotensin-(1-7) receptors, [D-alanine-7]-angiotensin-(1-7) (A-779, 1 mu M), influenced the response to angiotensin-(1-7). In conclusion, in the isolated guinea pig heart angiotensin-(1-7) induces coronary vasodilation that is mediated by endogenous bradykinin and subsequent stimulation of nitric oxide release through endothelial B-2 receptors. In contrast to other vascular beds, AT(2) angiotensin receptors and specific angiotensin-(1-7) receptors do not appear involved in angiotensin-(1-7)-induced coronary vasodilation in the isolated guinea pig heart.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据