上皮钠通道
内分泌学
内科学
肾素-血管紧张素系统
血管紧张素II
受体
阿米洛利
信使核糖核酸
敌手
下调和上调
髓腔
化学
医学
肾
钠
血压
基因
有机化学
生物化学
作者
Kexin Peng,Xiaohan Lu,Fei Wang,Adam Nau,Chao Ren,Shu Feng Zhou,Tianxin Yang
出处
期刊:American Journal of Physiology-renal Physiology
[American Physiological Society]
日期:2017-02-01
卷期号:312 (2): F245-F253
被引量:61
标识
DOI:10.1152/ajprenal.00178.2016
摘要
The (pro)renin receptor (PRR) is abundantly expressed in the collecting duct (CD) and the expression is further induced by angiotensin II (ANG II). The present study was conducted to investigate the role of CD PRR during ANG II-induced hypertension and to further explore the underlying mechanism. Radiotelemetry demonstrated that a 1-wk ANG II infusion gradually and significantly induced hypertensive response in floxed mice and this response was significantly attenuated in mice lacking PRR in the CD (termed CD PRR KO). ANG II infusion in floxed mice increased urinary renin activity and selectively induced renal medullary α-epithelial sodium channel (α-ENaC) mRNA and protein expression, all of which were blunted in the null mice. In cultured mpkCCD cells grown in Transwells, transepithelial Na+ transport as measured by using a volt-ohmmeter was transiently stimulated by acute ANG II treatment, which was abolished by a PRR antagonist, PRO20. In a chronic setting, ANG II treatment induced α-ENaC mRNA expression in mpkCCD cells, which was similarly blocked by PRO20. Chronic intramedullary infusion of an ENaC inhibitor amiloride in rats significantly attenuated ANG II-induced hypertension. Overall, the present study suggests that CD PRR contributes to ANG II-induced hypertension at least partially via activation of renal medullary ENaC.
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