Wulff Peer, Vallon Volker, Huang Dan Yang, Völkl Harald, Yu Fang, Richter Kerstin, Jansen Martina, Schlünz Michaela, Klingel Karin, Loffing Johannes, Kauselmann Gunther, Bösl Michael R, Lang Florian, Kuhl Dietmar
Zentrum für Molekulare Neurobiologie, University of Hamburg, Hamburg, Germany.
J Clin Invest. 2002 Nov;110(9):1263-8. doi: 10.1172/JCI15696.
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.
血清和糖皮质激素调节激酶（sgk1）由盐皮质激素诱导，进而上调非洲爪蟾卵母细胞中异源表达的肾上皮钠通道（ENaC）活性。因此，Sgk1被认为介导盐皮质激素对肾ENaC活性的刺激作用及抗利尿作用。在此我们表明，在标准氯化钠摄入量情况下，sgk1基因敲除（sgk1(-/-)）小鼠和野生型（sgk1(+/+)）小鼠的肾水和电解质排泄没有差异。相反，饮食中限制氯化钠摄入时，尽管血浆醛固酮水平升高、近端小管钠和液体重吸收增加，以及血压和肾小球滤过率降低，但sgk1(-/-)小鼠充分减少钠排泄的能力受损。
