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Am J Physiol Renal Physiol. 2018 Sep 1;315(3):F607-F617. doi: 10.1152/ajprenal.00122.2018. Epub 2018 May 23.

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

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Division of Nephrology and Hypertension, University of Utah Health Sciences Center , Salt Lake City, Utah.
Department of Cellular and Integrative Physiology, University of Texas Health Science Center , San Antonio, Texas.
Department of Veterans Affairs Medical Center , Salt Lake City, Utah.


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.


ENaC; collecting duct; prorenin receptor; sodium transport; water transport

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