Dietary salt regulates renal SGK1 abundance: relevance to salt sensitivity in the Dahl rat

M Farjah, BP Roxas, DL Geenen, RS Danziger - Hypertension, 2003 - Am Heart Assoc
Hypertension, 2003Am Heart Assoc
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 …
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.
Am Heart Assoc