Karger Publishers, Kidney and Blood Pressure Research, 4(31), p. 280-289, 2008
DOI: 10.1159/000151666
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<i>Background/Aims:</i> The serum- and glucocorticoid-inducible kinase SGK1 was originally cloned as a glucocorticoid-regulated gene and later as a transcriptional target for mineralocorticoids. SGK1 regulates channels and transporters including the renal Na<sup>+</sup> channel ENaC. It contributes to mineralocorticoid regulation of renal Na<sup>+</sup> excretion and salt appetite. The present study explored the contribution of SGK1 to effects of glucocorticoids on mineral and electrolyte metabolism. <i>Methods:</i> SGK1-knockout mice (<i>sgk1</i><sup>–/–</sup>) and their wild-type littermates (<i>sgk1</i><sup>+/+</sup>) were analyzed in metabolic cages with or without treatment for 14 days with dexamethasone (3 mg/kg b.w., i.p.). Blood pressure was determined by the tail-cuff method. <i>Results:</i> Prior to treatment fluid intake, urinary flow rate, urinary Na<sup>+</sup>, K<sup>+</sup>, phosphate and Cl<sup>–</sup> excretion, plasma electrolyte and glucose concentrations as well as blood pressure were similar in <i>sgk1</i><sup>–/–</sup> and<i> sgk1</i><sup>+/+</sup> mice. Dexamethasone did not significantly alter renal Na<sup>+</sup>, K<sup>+</sup>, Cl<sup>–</sup> and Ca<sup>2+</sup> excretion but decreased plasma Ca<sup>2+</sup> and phosphate concentration in <i>sgk1</i><sup>+/+</sup> mice. The effect on Ca<sup>2+</sup> was significantly augmented and the effect on phosphate significantly blunted in <i>sgk1</i><sup>–/–</sup> mice. Dexamethasone significantly increased fasting blood glucose concentrations in both genotypes. Dexamethasone increased blood pressure in <i>sgk1</i><sup>+/+</sup> mice, an effect significantly blunted in <i>sgk1</i><sup>–/–</sup> mice. <i>Conclusions:</i> The present observations disclose SGK1-sensitive glucocorticoid effects on calcium-phosphate metabolism and blood pressure.