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

May 24, 2018American journal of physiology. Renal physiology

The prorenin receptor in main kidney duct cells controls salt and water balance, but not in other duct cells

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Abstract

PC knockout mice showed reduced renal medullary ENaC-α abundance and increased urinary Na losses on a low-Na diet compared to controls.

Principal cells (PC) play a significant role in regulating ENaC activity and water transport through prorenin receptor (PRR).
Intercalated cell (IC) PRR deletion did not affect sodium balance or ENaC abundance.
Acute prorenin treatment increased ENaC channel numbers and open probability in control and IC PRR KO mice, but not in PC PRR KO mice.
PC KO mice exhibited increased urine volume, reduced urine osmolality, and decreased abundance of renal medullary AQP2 compared to controls.

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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 Nachannel (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 Naand 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 HATPase promoters, respectively. PC KO mice had reduced renal medullary ENaC-α abundance and increased urinary Nalosses on a low-Nadiet compared with controls. Conversely, IC KO mice had no apparent differences in Nabalance 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 Naexcretion, and water transport. + + + + + + +

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

Abstract

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