Role of serum- and glucocorticoid-inducible kinase SGK1 in glucocorticoid regulation of renal electrolyte excretion and blood pressure.
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Role of serum- and glucocorticoid-inducible kinase SGK1 in glucocorticoid regulation of renal electrolyte excretion and blood pressure. / Boini, Krishna M; Nammi, Srinivas; Grahammer, Florian; Osswald, Hartmut; Kuhl, Dietmar; Lang, Florian.
in: KIDNEY BLOOD PRESS R, Jahrgang 31, Nr. 4, 4, 2008, S. 280-289.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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T1 - Role of serum- and glucocorticoid-inducible kinase SGK1 in glucocorticoid regulation of renal electrolyte excretion and blood pressure.
AU - Boini, Krishna M
AU - Nammi, Srinivas
AU - Grahammer, Florian
AU - Osswald, Hartmut
AU - Kuhl, Dietmar
AU - Lang, Florian
PY - 2008
Y1 - 2008
N2 - BACKGROUND/AIMS: 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(+) channel ENaC. It contributes to mineralocorticoid regulation of renal Na(+) excretion and salt appetite. The present study explored the contribution of SGK1 to effects of glucocorticoids on mineral and electrolyte metabolism. METHODS: SGK1-knockout mice (sgk1(-/-)) and their wild-type littermates (sgk1(+/+)) 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. RESULTS: Prior to treatment fluid intake, urinary flow rate, urinary Na(+), K(+), phosphate and Cl(-) excretion, plasma electrolyte and glucose concentrations as well as blood pressure were similar in sgk1(-/-) and sgk1(+/+) mice. Dexamethasone did not significantly alter renal Na(+), K(+), Cl(-) and Ca(2+) excretion but decreased plasma Ca(2+) and phosphate concentration in sgk1(+/+) mice. The effect on Ca(2+) was significantly augmented and the effect on phosphate significantly blunted in sgk1(-/-) mice. Dexamethasone significantly increased fasting blood glucose concentrations in both genotypes. Dexamethasone increased blood pressure in sgk1(+/+) mice, an effect significantly blunted in sgk1(-/-) mice. CONCLUSIONS: The present observations disclose SGK1-sensitive glucocorticoid effects on calcium-phosphate metabolism and blood pressure.
AB - BACKGROUND/AIMS: 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(+) channel ENaC. It contributes to mineralocorticoid regulation of renal Na(+) excretion and salt appetite. The present study explored the contribution of SGK1 to effects of glucocorticoids on mineral and electrolyte metabolism. METHODS: SGK1-knockout mice (sgk1(-/-)) and their wild-type littermates (sgk1(+/+)) 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. RESULTS: Prior to treatment fluid intake, urinary flow rate, urinary Na(+), K(+), phosphate and Cl(-) excretion, plasma electrolyte and glucose concentrations as well as blood pressure were similar in sgk1(-/-) and sgk1(+/+) mice. Dexamethasone did not significantly alter renal Na(+), K(+), Cl(-) and Ca(2+) excretion but decreased plasma Ca(2+) and phosphate concentration in sgk1(+/+) mice. The effect on Ca(2+) was significantly augmented and the effect on phosphate significantly blunted in sgk1(-/-) mice. Dexamethasone significantly increased fasting blood glucose concentrations in both genotypes. Dexamethasone increased blood pressure in sgk1(+/+) mice, an effect significantly blunted in sgk1(-/-) mice. CONCLUSIONS: The present observations disclose SGK1-sensitive glucocorticoid effects on calcium-phosphate metabolism and blood pressure.
U2 - 10.1159/000151666
DO - 10.1159/000151666
M3 - SCORING: Zeitschriftenaufsatz
VL - 31
SP - 280
EP - 289
JO - KIDNEY BLOOD PRESS R
JF - KIDNEY BLOOD PRESS R
SN - 1420-4096
IS - 4
M1 - 4
ER -