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

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...

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Bibliographic Details
Published in:Hypertension (Dallas, Tex. 1979) Tex. 1979), 2003-04, Vol.41 (4), p.874-878
Main Authors: Farjah, Mariam, Roxas, Bryan P, Geenen, David L, Danziger, Robert S
Format: Article
Language:English
Subjects:
Administration, Oral
Aldosterone - blood
Animals
Arterial hypertension. Arterial hypotension
Biological and medical sciences
Blood and lymphatic vessels
Blood Pressure
Cardiology. Vascular system
Experimental diseases
Gene Expression Regulation
Hypertension - genetics
Hypertension - metabolism
Hypertension - physiopathology
Immediate-Early Proteins
Kidney - drug effects
Kidney - metabolism
Male
Medical sciences
Nuclear Proteins
Protein-Serine-Threonine Kinases - genetics
Protein-Serine-Threonine Kinases - metabolism
Rats
Rats, Inbred Dahl
Rats, Sprague-Dawley
RNA, Messenger - biosynthesis
Sodium Chloride - administration & dosage
Sodium Chloride - pharmacology
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Summary: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
ISSN:0194-911X
1524-4563
DOI:10.1161/01.HYP.0000063885.48344.EA