血管紧张素Ⅱ2型受体对血管和肾脏功能的影响  

Effects of Angiotensin Ⅱ Type 2 Receptor on Vascular and Renal Action

作　　者：孙红周（综述）[1] 卞钊（审校）[1] 

机构地区：[1]广西医科大学附属第一医院心血管研究所,南宁530021

出　　处：《医学综述》2007年第5期382-384,共3页Medical Recapitulate

摘　　要：肾素-血管紧张素系统(RAS)是机体调节血压和肾脏排钠的重要功能系统,其效应分子血管紧张素Ⅱ主要包括两种受体血管紧张素Ⅱ1型受体(AT1)和血管紧张素Ⅱ2型受体(AT2)。血管紧张素Ⅱ的主要功能是通过AT1受体介导的。现在越来越多的研究表明AT2受体有拮抗AT1受体的作用主要表现在血管舒张方面。近几年来研究表明AT2受体的微血管舒张作用是通过缓激肽相关或无关的方式产生NO来介导。虽然AT2受体在肾脏的近端小管、远端小管和血管系统都存在表达,AT2受体刺激诱导肾脏的缓激肽(bradykinin)/NO通道,但很少有关AT2受体调节肾功能和钠外排方面有价值的研究。现就近年来对AT2受体在血管舒张和肾功能的影响方面的最新研究进展简要综述。the renin-angiotensin system is an important system in regulating blood pressure and renal sodium excretion, its effective component angiotensin Ⅱ mainly includes two receptors of AT1 and AT2. While the majority of angiotensin Ⅱ actions are mediated via the AT1 receptor, More and more evidences showed that the AT2 receptor has its inbibitory effect to that of AT1 mainly in vasodilation. Micmvascular dilatation of AT2 receptor can be achieved by NO with or without bradykinin. Although the AT2 receptor is expressed in renal proximal and distal tubules and vasculature, and AT2 receptor stimulation induces a bradykinin/NO pathway within the kidney, little information is available concerning AT2 receptor regulation of renal function and sodium excretion. This article summarized related progress of its role in vascular and renal actions.

关 键 词：血管紧张素Ⅱ AT1受体 AT2受体 血管 肾 

分 类 号：R344.1[医药卫生—基础医学] R331.32