{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,28]],"date-time":"2026-05-28T01:22:01Z","timestamp":1779931321567,"version":"3.53.1"},"reference-count":29,"publisher":"S. Karger AG","issue":"2","license":[{"start":{"date-parts":[[2009,1,1]],"date-time":"2009-01-01T00:00:00Z","timestamp":1230768000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"},{"start":{"date-parts":[[2009,1,1]],"date-time":"2009-01-01T00:00:00Z","timestamp":1230768000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Kidney Blood Press Res"],"published-print":{"date-parts":[[2009]]},"abstract":"<i>Background\/Aims:<\/i> Serum- and glucocorticoid-inducible kinase 1 (SGK1) stimulates the epithelial sodium channel (ENaC), renal outer medullary K<sup>+<\/sup> channel 1, Na<sup>+<\/sup>\/K<sup>+<\/sup>-ATPase and presumably the Na<sup>+<\/sup>-Cl<sup>\u2013<\/sup> cotransporter (NCC). SGK1-deficient mice (<i>sgk<\/i><sup>\u2013\/\u2013<\/sup>) show a compensated salt-losing phenotype with secondary hyperaldosteronism. The present experiments explored the role of SGK1 in the response to diuretics. <i>Methods:<\/i><i>sgk1<\/i><sup>\u2013\/\u2013<\/sup> mice and their wild-type littermates (<i>sgk1<\/i><sup>+\/+<\/sup>) were treated with the ENaC blocker triamterene (200 mg\/l), the Na<sup>+<\/sup>-K<sup>+<\/sup>-2Cl<sup>\u2013<\/sup> cotransport inhibitor furosemide (125 mg\/l), the NCC blocker hydrochlorothiazide (400 mg\/l) and the mineralocorticoid receptor blocker canrenoate (800 mg\/l) for 8 days. Renal SGK1 expression was studied using quantitative RT-PCR and immunofluorescence. <i>Results:<\/i> Diuretic treatment increased SGK1 mRNA and protein expression in the kidney of wild-type <i>sgk1<\/i><sup>+\/+<\/sup> mice. The responses to furosemide, hydrochlorothiazide or canrenoate were not different between <i>sgk1<\/i><sup>+\/+<\/sup> and <i>sgk1<\/i><sup>\u2013\/\u2013<\/sup> mice, and were accompanied by moderate increases in plasma aldosterone and urea concentrations. However, treatment with triamterene in <i>sgk1<\/i><sup>\u2013\/\u2013<\/sup> mice (but not in <i>sgk1<\/i><sup>+\/+<\/sup> mice) led to severe, eventually lethal, body weight loss as well as increases in plasma aldosterone, urea and K<sup>+<\/sup> concentrations. <i>Conclusions:<\/i> SGK1 is required for diuretic tolerance to triamterene. The observations confirm the impaired kaliuretic potency of <i>sgk1<\/i><sup>\u2013\/\u2013<\/sup> mice and point to a role of SGK1 in renal Na<sup>+<\/sup> reabsorption by mechanisms other than ENaC.<\/jats:p>","DOI":"10.1159\/000214439","type":"journal-article","created":{"date-parts":[[2009,4,24]],"date-time":"2009-04-24T13:41:27Z","timestamp":1240580487000},"page":"119-127","source":"Crossref","is-referenced-by-count":16,"title":["Responses to Diuretic Treatment in Gene-Targeted Mice Lacking Serum- and Glucocorticoid-Inducible Kinase 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