Peer Wulff, Volker Vallon, Dan Yang Huang, Harald Völkl, Fang Yu, Kerstin Richter, Martina Jansen, Michaela Schlünz, Karin Klingel, Johannes Loffing, Gunther Kauselmann, Michael R. Bösl, Florian Lang, Dietmar Kuhl
J Clin Invest.
2002;
110(9):1263–1268
doi:10.1172/JCI15696
This article Copyright © 2002, The American Society for Clinical Investigation
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T
he serum- and glucocorticoid-regulated kinase (sgk1) is induced by mineralocorticoids and, in turn, upregulates heterologously expressed renal epithelial Na+ channel (ENaC) activity in Xenopus oocytes. Accordingly, Sgk1 is considered to mediate the mineralocorticoid stimulation of renal ENaC activity and antinatriuresis. Here we show that at standard NaCl intake, renal water and electrolyte excretion is indistinguishable in sgk1-knockout (sgk1–/–) mice and wild-type (sgk1+/+) mice. In contrast, dietary NaCl restriction reveals an impaired ability of sgk1–/– mice to adequately decrease Na+ excretion despite increases in plasma aldosterone levels and proximal-tubular Na+ and fluid reabsorption, as well as decreases in blood pressure and glomerular filtration rate.
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