Impaired renal Na+retention in the sgk1-knockout mouse

Peer Wulff, V. Vallon, D. Y. Huang, H. Volkl, F. Yu, K. Richter, M. Jansen, M. Schlunz, K. Klingel, J. Loffing, G. Kauselmann, M. R. Bosel, F. Lang, D. Kuhl

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Abstract

The 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.

Original languageEnglish
Pages (from-to)1263-1268
Number of pages5
JournalThe Journal of Clinical Investigation
Volume110
Issue number9
DOIs
Publication statusPublished - Nov 2002

Keywords

  • EPITHELIAL SODIUM-CHANNEL
  • THREONINE PROTEIN-KINASE
  • LUNG LIQUID CLEARANCE
  • PSEUDOHYPOALDOSTERONISM TYPE-1
  • TRANSCRIPTIONAL REGULATION
  • PROXIMAL TUBULE
  • BETA-SUBUNIT
  • CELL-VOLUME
  • SGK
  • ENAC

Cite this

Wulff, P., Vallon, V., Huang, D. Y., Volkl, H., Yu, F., Richter, K., Jansen, M., Schlunz, M., Klingel, K., Loffing, J., Kauselmann, G., Bosel, M. R., Lang, F., & Kuhl, D. (2002). Impaired renal Na+retention in the sgk1-knockout mouse. The Journal of Clinical Investigation, 110(9), 1263-1268. https://doi.org/10.1172/JCI200215696