| First Author | Peng K | Year | 2017 |
| Journal | Am J Physiol Renal Physiol | Volume | 312 |
| Issue | 2 | Pages | F245-F253 |
| PubMed ID | 27122543 | Mgi Jnum | J:280034 |
| Mgi Id | MGI:6367462 | Doi | 10.1152/ajprenal.00178.2016 |
| Citation | Peng K, et al. (2017) Collecting duct (pro)renin receptor targets ENaC to mediate angiotensin II-induced hypertension. Am J Physiol Renal Physiol 312(2):F245-F253 |
| abstractText | 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 alpha-epithelial sodium channel (alpha-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 alpha-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. |
