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J Am Soc Nephrol 15:885-891, 2004
© 2004 American Society of Nephrology

BASIC SCIENCE

Impaired Regulation of Renal K+ Elimination in the sgk1-Knockout Mouse

Dan Yang Huang*,{dagger}, Peer Wulff{ddagger}, Harald Völkl||, Johannes Loffing, Kerstin Richter*,#, Dietmar Kuhl§, Florian Lang{dagger} and Volker Vallon*,#

Departments of *Pharmacology and {dagger}Physiology I, University of Tübingen, {ddagger}Department of Clinical Neurobiology, University of Heidelberg, and §Department of Biology, Chemistry and Pharmacy, Free University of Berlin, Germany; ||Department of Physiology, University of Innsbruck, Austria; Institute of Anatomy, University of Zürich, Switzerland; and #Departments of Medicine and Pharmacology, University of California, San Diego and VAMCSD, San Diego, California.

Correspondence to: Dr. Volker Vallon, Division of Nephrology/Hypertension, Departments of Medicine and Pharmacology, University of California San Diego and VAMC, 3350 La Jolla Village Drive (9151), San Diego, CA 92161. Phone: 858-552-8585 ext. 5945; Fax: 858-642-1438, E-mail: vvallon{at}ucsd.edu

ABSTRACT. Serum- and glucocorticoid-regulated kinase 1 (Sgk1) contributes to Na+ reabsorption in the aldosterone-sensitive distal nephron. Sgk1-knockout (sgk1-/-) and littermate wild-type mice (sgk1+/+) were used to test the importance of Sgk1 in renal elimination of K+. Intravenous application of K+ load under anesthesia increased plasma K+ concentration by 1.3 to 1.4 mM in both sgk1-/- (n = 6) and sgkl+/+ (n = 7) mice. However, the increase of absolute and fractional renal K+ excretion observed in sgk1+/+ was significantly blunted in sgk1-/- animals. Both groups of mice decreased or increased renal K+ excretion to a similar extent after a low (<0.03%) or high (5%) K+ diet for 6 d, respectively. In sgk1+/+, plasma K+ concentration was not significantly modified by either high or low K+ diet. In sgk1-/-, however, high K+ diet enhanced plasma K+ concentration by about 1.6 mM, despite an excessive increase of plasma aldosterone concentration reaching values about sixfold higher than in sgk1+/+. Electrophysiological and immunohistochemical studies under high K+ diet indicated that reduced epithelial Na+ channel ENaC and/or Na+/K+-ATPase activity in the aldosterone-sensitive distal nephron accounted for the impaired response in sgk1-/- and that an enhanced apical abundance of renal outer medullary K+ channel ROMK partly compensated for the defect. The acute and chronic regulation of renal K+ elimination involves Sgk1.




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