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• W2785319551 abstract "The Na + -Cl − cotransporter (NCC) in distal convoluted tubule (DCT) plays important roles in renal NaCl reabsorption. The current hypothesis for the mechanism of regulation of NCC focuses on WNK4 and intracellular Cl − concentration ([Cl − ] i ). WNK kinases bind Cl − , and Cl − binding decreases the catalytic activity. It is believed that hypokalemia under low K + intake decreases [Cl − ] i to activate WNK4, which thereby phosphorylates and stimulates NCC through activation of SPAK. However, increased NCC activity and apical NaCl entry would mitigate the fall in [Cl − ] i. Whether [Cl − ] i in DCT under low-K + diet is sufficiently low to activate WNK4 is unknown. Furthermore, increased luminal NaCl delivery also stimulates NCC and causes upregulation of the transporter. Unlike low K + intake, increased luminal NaCl delivery would tend to increase [Cl − ] i . Thus we investigated the role of WNK4 and [Cl − ] i in regulating NCC. We generated Wnk4-knockout mice and examined regulation of NCC by low K + intake and by increased luminal NaCl delivery in knockout (KO) and wild-type mice. Wnk4-KO mice have marked reduction in the abundance, phosphorylation, and functional activity of NCC vs. wild type. Low K + intake increases NCC phosphorylation and functional activity in wild-type mice, but not in Wnk4-KO mice. Increased luminal NaCl delivery similarly upregulates NCC, which, contrary to low K + intake, is not abolished in Wnk4-KO mice. The results reveal that modulation of WNK4 activity by [Cl − ] i is not the sole mechanism for regulating NCC. Increased luminal NaCl delivery upregulates NCC via yet unknown mechanism(s) that may override inhibition of WNK4 by high [Cl − ] i ." @default.
• W2785319551 created "2018-02-23" @default.
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• W2785319551 date "2018-05-01" @default.
• W2785319551 modified "2023-10-14" @default.
• W2785319551 title "Differential roles of WNK4 in regulation of NCC in vivo" @default.
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• W2785319551 doi "https://doi.org/10.1152/ajprenal.00177.2017" @default.
• W2785319551 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6031911" @default.
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