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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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