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Endocrinology Vol. 142, No. 4 1587-1594
Copyright © 2001 by The Endocrine Society

ARTICLES

The Serum- and Glucocorticoid-Induced Kinase Is a Physiological Mediator of Aldosterone Action1

Aditi Bhargava, Meryl J. Fullerton, Kathy Myles, Timothy M. Purdy, John W. Funder, David Pearce and Timothy J. Cole

Baker Medical Research Institute (M.J.F., K.M., J.W.F., T.J.C.), Melbourne 8008, Australia; and Department of Medicine, University of California (A.B., T.M.P., D.P.), San Francisco, California 94143

Address all correspondence and requests for reprints to: Dr. David Pearce, Department of Medicine, Box 0532, 513 Parnassus Avenue, University of California, San Francisco, California 94143. E-mail: pearced{at}medicine.ucsf.edu

Aldosterone plays a major role in regulating sodium and potassium flux in epithelial tissues such as kidney and colon. Recent evidence suggests that serum- and glucocorticoid-regulated kinase (SGK) is induced by aldosterone and acts as a key mediator of aldosterone action in epithelial tissues. Induction of SGK messenger RNA (mRNA) has previously been shown within 30 min of addition of supraphysiological doses of aldosterone to Xenopus A6 cells and within 4 h in rat kidney in vivo. In this study we determined the time course of SGK induction, at doses of aldosterone in the physiological range, in rat kidney and colon, using Northern and Western blot analyses and in situ hybridization and determined concurrent changes in urinary sodium and potassium excretion by Kagawa bioassay. On Northern blot analysis, SGK mRNA levels were significantly elevated in both kidney and colon 60 min after the injection of aldosterone. SGK protein in late distal colon was significantly elevated 2 and 4 h after aldosterone treatment. In situ hybridization showed SGK mRNA to be induced in renal collecting ducts and distal tubular elements in both cortex and medulla by doses of aldosterone of 0.1 µg/100 g BW or more within 30 min of steroid treatment. Significant changes in urinary composition were similarly seen with an aldosterone dose of 0.1 µg/100 g BW from 90 min after aldosterone injection. The early onset of SGK induction in kidney and colon and the correlation with urinary changes in terms of both time course and dose response suggest that SGK plays an important role in mediating the effects of aldosterone on sodium homeostasis in vivo.




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