Published Online
on March 17, 2003

A more recent version of this article appeared on April 1, 2003

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Submitted on October 23, 2002
Revised on November 15, 2002

Dietary Salt Regulates Renal SGK1 Abundance. Relevance to Salt Sensitivity in the Dahl Rat

Mariam Farjah; Bryan P. Roxas; David L. Geenen; and Robert S. Danziger^*

From the Section of Cardiology, Department of Medicine, University of Illinois at Chicago (M.F., B.P.R., D.L.G., R.S.D.), Chicago, Ill; and West Side Division Veterans Administration Chicago Health Care System (M.F., B.P.R., R.S.D.), Chicago, Ill.

^* To whom correspondence should be addressed. E-mail: Rdanziger{at}aol.com.

Abstract--Serum and glucocorticoid-induced kinase 1 (SGK1) activates the epithelial sodium channel (eNaC) in tubules. We examined renal SGK1 abundance in salt-adaptation and in salt-sensitive hypertension. Sprague-Dawley and Dahl salt-sensitive rats were placed on either 8% or 0.3% NaCl diets for 10 days. Plasma aldosterone levels were 2.5-fold greater on 0.3% versus 8% NaCl diets in both rat strains. Both serum and glucocorticoid-induced kinase 1 transcript and protein abundance were less (P<0.01) in Sprague-Dawley rats and greater (P<0.01) in Dahl salt-sensitive rats on 8% versus 0.3% NaCl diets. The cDNA sequences of serum and glucocorticoid-induced kinase 1 in both strains of rat were the same. The present results provide evidence that the abundance of serum and glucocorticoid-induced kinase 1 in rat kidney may play a role in salt adaptation and the pathogenesis of hypertension and suggests that aldosterone is not the primary inducer of SGK1 in the Sprague-Dawley rat.

Key words: aldosterone • rat, Dahl • glucocorticoids • kinase • hypertension, renal • sodium, dietary • blood pressure

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