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- W404191146 abstract "Constitutive Nedd4-2 knockout (KO) mice show Na+ retention and salt-sensitive hypertension. To determine the role of renal Nedd4-2 in adult mice, we generated inducible renal tubule-specific Nedd4-2 KO mice (Nedd4-2Pax8/LC1) using a combination of the Tet-On and Cre-loxP systems. Under standard and high-Na+ diets, KO displayed decreased plasma aldosterone but normal Na+/K+ balance. Under high Na+ diet, KO mice showed hypercalciuria and hypertension, both treated by thiazides. NCC expression and phosphorylation were increased in the KO. Interestingly, KO showed increased intracellular β- and γENaC abundance, but decreased α- and γENaC proteolytic cleavage and decreased αENaC mRNA and protein expression, suggesting down-regulated ENaC. In contrast, ROMK protein expression and cell surface localization were increased in the distal convoluted tubules and connecting tubules of KO, in keeping with the absence of hyperkalemia. Thus, in adult mice, loss of renal Nedd4-2 causes a pseudohypoaldosteronism type II-like syndrome with NCC up-regulation leading to salt-sensitive hypertension and hypercalciuria, suggesting that Nedd4-2 primarily targets NCC. The accompanying hypoaldosteronism with down-regulation of ENaC-mediated Na+ reabsorption together with an up-regulation of K+ secretion via ROMK likely contributes to the compensated phenotype of the KO mice and explains the maintained Na+/K+ balance." @default.
- W404191146 created "2016-06-24" @default.
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- W404191146 date "2012-04-01" @default.
- W404191146 modified "2023-09-26" @default.
- W404191146 title "Loss of renal Nedd4‐2 in adult mice leads to PHAII compensated by ENaC down‐regulation and ROMK up‐regulation" @default.
- W404191146 doi "https://doi.org/10.1096/fasebj.26.1_supplement.1067.2" @default.
- W404191146 hasPublicationYear "2012" @default.
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