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血管紧张素Ⅱ2型受体基因缺失不影响肾素-血管紧张素系统

李文歌, 陈香美, 叶一舟, 张颖, 于力方

解放军总医院肾科. 北京

摘要

基于目前对血管紧张素Ⅱ2型受体（AT2）功能的认识，认为血管紧张素Ⅱ1型受体（AT1）和AT2受体有相互拮抗作用。依据上述论点，本研究利用AT2受体基因敲出小鼠，观察了AT2受体缺失后是否造成肾素-血管紧张素系统其它成分代偿性紊乱。结果发现，AT2受体基因缺失小鼠血浆和肾组织中血管紧张素Ⅱ的浓度以及肾组织中肾素、AT1A受体的基因表达均未发生明显改变，表明AT2受体缺失未对肾素-血管紧张素系统产生显著影响，AT2受体的功能已被代偿，但代偿途径尚有待于进一步研究。

关键词： AT2受体; 基因缺失; 肾素-血管紧张素系统

Cui Hong

First Clinical Institute，China Medical University. Shenyang 110001,Liaoning, China

Abstract

It has been postulated that Angiotensin Ⅱ type 2 receptor (AT2) functionally antagonizes ac 1 (AT1) receptor. In the present study, we investigated whether gene deletion of AT2 receptor causes the compensatory chaos of renin-angiotensin system in mice. It was shown that the concentrations of Angiotensin Ⅱ in plasma and kidney tissues and the expressions of renin and AT1A receptor in the AT2 gene null face were unchanged, as compared with those in AT2 wild-type mice. Thiss result suggests that gene deletion of AT2 receptor does not markeddly impact the stability of renin-angiotensin system all the inductive function of AT2 receptor is compensated in a way remaining to be clarified.

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引用本文：

李文歌, 陈香美, 叶一舟, 张颖, 于力方. 血管紧张素Ⅱ2型受体基因缺失不影响肾素-血管紧张素系统 [J]. 生理学报 1998; 50 (4): .

Cui Hong. . Acta Physiol Sin 1998; 50 (4): (in Chinese with English abstract).