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

CA Bickel, JG Verbalis, MA Knepper… - American Journal of …, 2001 - journals.physiology.org
American Journal of Physiology-Renal Physiology, 2001journals.physiology.org
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 …
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 α1-subunit of Na-K-ATPase, the thiazide-sensitive Na-Cl cotransporter (NCC or TSC), and the β-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 α-subunit of ENaC. These selective increases could possibly increase sodium retention by the kidney and therefore could play a role in obesity-related hypertension.
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