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血管紧张素II通过2型受体诱导的血管舒张：缓激肽和一氧化氮的作用

Angiotensin II-induced vasodilation via type 2 receptor: role of bradykinin and nitric oxide.

作者信息

Yayama Katsutoshi, Okamoto Hiroshi

机构信息

Laboratory of Cardiovascular Pharmacology, Department of Biopharmaceutical Sciences, Kobe Gakuin University, Minatojima 1-1-3, Chuo-ku, Kobe 650-8586, Japan.

出版信息

Int Immunopharmacol. 2008 Feb;8(2):312-8. doi: 10.1016/j.intimp.2007.06.012. Epub 2007 Jul 19.

DOI:10.1016/j.intimp.2007.06.012
PMID:18182246
Abstract

Angiotensin II (Ang II) plays important roles in the regulation of cardiovascular functions and diseases mainly via the type 1 (AT1) receptor. In contrast, recent studies have shown that the actions of Ang II via the type 2 (AT2) receptor are counter-regulatory to those mediated via the AT1 receptor. Using an animal model of hypertension, we have demonstrated that Ang II produces a vasodilator effect through the AT2 receptor via the bradykinin (BK)-dependent activation of endothelial nitric oxide (NO) synthase. In this review, we focus on the role of BK and NO in AT2-receptor-mediated vasodilation.

摘要

血管紧张素II（Ang II）主要通过1型（AT1）受体在心血管功能调节和疾病发生中发挥重要作用。相比之下，最近的研究表明，Ang II通过2型（AT2）受体所产生的作用与通过AT1受体介导的作用具有反向调节关系。利用高血压动物模型，我们已经证明，Ang II通过缓激肽（BK）依赖性激活内皮型一氧化氮合酶，经AT2受体产生血管舒张作用。在这篇综述中，我们重点关注BK和NO在AT2受体介导的血管舒张中的作用。

相似文献

[1]
Angiotensin II-induced vasodilation via type 2 receptor: role of bradykinin and nitric oxide.

Int Immunopharmacol. 2008-2

[2]
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[3]
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[4]
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[6]
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[7]
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[8]
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[10]
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[3]
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[4]
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[5]
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[6]
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[7]
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[9]
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[10]
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