Compensatory role for Sgk2 mediated sodium reabsorption during salt deprivation in Sgk1 knockout mice.

The purpose of this study was to investigate the role of Sgk2 in the regulation of salt and water homeostasis. Kidney function and expression of Sgk1, Sgk2, Sgk3, and aENaC were determined during normal and 0% salt intake in Sgk1-/-,Sgk2-/-, and Sgk1-/-,Sgk2-/- double KO mice (DKO). During normal salt intake, renal function of Sgk1-/-, Sgk2-/- and DKO mice were similar to wild type mice. The renal response to salt deprivation was impaired in Sgk1-/- but not in Sgk2-/- mice. DKO mice on 0% salt diet gained less body weight, had higher urine flow, sodium and chloride excretions, and similar glomerular filtration rate than Sgk1+/+,Sgk2+/+ mice. Plasma concentrations of sodium, chloride and potassium were increased, renal cortical Sgk3 expression was increased, and there was no difference in renal αENaC expression in DKO compared to wild type mice. DKO mice had an impaired ability to reabsorb water, sodium, chloride, and potassium during salt deprivation compared to Sgk1-/-or Sgk2-/- mice. In conclusion, Sgk2 has a minimal role in the regulation of salt and water homeostasis during normal or reduced salt intake in vivo. However, Sgk2 significantly contributes to water and electrolyte homeostasis during salt deprivation in the absence of Sgk1, suggesting that Sgk2 can compensate for functional changes in Sgk1. [ABSTRACT FROM AUTHOR]