Collecting duct principal, but not intercalated, cell prorenin receptor regulates renal sodium and water excretion

Nirupama Ramkumar, Deborah Stuart, Elena Mironova, Nikita Abraham, Yang Gao, Shuping Wang, Jayalakshmi Lakshmipathi, James D. Stockand, Donald E. Kohan

Research output: Contribution to journalArticlepeer-review

10 Scopus citations

Abstract

The collecting duct is the predominant nephron site of prorenin and prorenin receptor (PRR) expression. We previously demonstrated that the collecting duct PRR regulates epithelial Na+ channel (ENaC) activity and water transport; however, which cell type is involved remains unclear. Herein, we examined the effects of principal cell (PC) or intercalated cell (IC) PRR deletion on renal Na+ and water handling. PC or IC PRR knockout (KO) mice were obtained by crossing floxed PRR mice with mice harboring Cre recombinase under the control of the AQP2 or B1 subunit of the H+ ATPase promoters, respectively. PC KO mice had reduced renal medullary ENaC-α abundance and increased urinary Na+ losses on a low-Na+ diet compared with controls. Conversely, IC KO mice had no apparent differences in Na+balance or ENaC abundance compared with controls. Acute treatment with prorenin increased ENaC channel number and open probability in acutely isolated cortical collecting ducts from control and IC PRR KO, but not PC PRR KO, mice. Furthermore, compared with controls, PC KO, but not IC KO mice, had increased urine volume, reduced urine osmolality, and reduced abundance of renal medullary AQP2. Taken together, these findings indicate that PC, but not IC, PRR modulates ENaC activity, urinary Na+ excretion, and water transport.

Original languageEnglish (US)
Pages (from-to)F607-F617
JournalAmerican Journal of Physiology - Renal Physiology
Volume315
Issue number3
DOIs
StatePublished - Sep 2018

Keywords

  • Collecting duct
  • ENaC
  • Prorenin receptor
  • Sodium transport
  • Water transport

ASJC Scopus subject areas

  • Physiology
  • Urology

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