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Am J Physiol Renal Physiol 281: F639-F648, 2001;
0363-6127/01 $5.00
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Vol. 281, Issue 4, F639-F648, October 2001

Increased renal Na-K-ATPase, NCC, and beta -ENaC abundance in obese Zucker rats

Crystal A. Bickel1, Joseph G. Verbalis1, Mark A. Knepper2, and Carolyn A. Ecelbarger1

Division of Endocrinology and Metabolism, 1 Department of Medicine, Georgetown University, Washington, District of Columbia 20007; and 2 Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892

Renal sodium retention, as a result of increased abundance of sodium transporters, may play a role in the development and/or maintenance of the increased blood pressure in obesity. To address this hypothesis, we evaluated the relative abundances of renal sodium transporters in lean and obese Zucker rats at 2 and 4 mo of age by semiquantitative immunoblotting. Mean systolic blood pressure was higher in obese rats relative to lean at 3 mo, P < 0.02. Furthermore, circulating insulin levels were 6- or 13-fold higher in obese rats compared with lean at 2 or 4 mo of age, respectively. The abundances of the alpha 1-subunit of Na-K-ATPase, the thiazide-sensitive Na-Cl cotransporter (NCC or TSC), and the beta -subunit of the epithelial sodium channel (ENaC) were all significantly increased in the obese rats' kidneys. There were no differences for the sodium hydrogen exchanger (NHE3), the bumetanide-sensitive Na-K-2Cl cotransporter (NKCC2 or BSC1), the type II sodium-phosphate cotransporter (NaPi-2), or the alpha -subunit of ENaC. These selective increases could possibly increase sodium retention by the kidney and therefore could play a role in obesity-related hypertension.

sodium-phosphate cotransporter type II; sodium-hydrogen exchanger type III; bumetanide-sensitive sodium-potassium-2 chloride cotransporter; insulin resistance; hypertension; sodium-chloride cotransporter; epithelial sodium channel; adenosine 5'-triphosphatase


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