Published online before print March 17, 2003, doi: 10.1161/01.HYP.0000063885.48344.EA
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(Hypertension. 2003;41:874.)
© 2003 American Heart Association, Inc.
Rapid Communication |
Dietary Salt Regulates Renal SGK1 Abundance
Relevance to Salt Sensitivity in the Dahl Rat
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.
Correspondence to Robert S. Danziger, MD, Department of Medicine, University of Illinois at Chicago, 840 S Wood St, Chicago, IL 60612. E-mail Rdanziger{at}aol.com
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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