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Am J Physiol Renal Physiol (November 22, 2005). doi:10.1152/ajprenal.00108.2005
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Submitted on March 21, 2005
Accepted on November 10, 2005

Regulation of Blood Pressure, the Epithelial Sodium Channel (ENaC), and other Key Renal Sodium Transporters by Chronic Insulin Infusion in Rats

Jian Song1, Xinqun Hu1, Shahla Riazi1, Swasti Tiwari1, James B. Wade2, and Carolyn A. Ecelbarger3*

1 Division of Endocrinology and Metabolism, Department of Medicine, Georgetown University, Washington, DC, USA
2 Department of Physiology, University of Maryland-Baltimore, Baltimore, MD, USA
3 Division of Endocrinology and Metabolism, Department of Medicine, Georgetown University, Washington, DC, USA; Center for Sex Differences, Georgetown University, Washington, DC, USA

* To whom correspondence should be addressed. E-mail: ecelbarc{at}georgetown.edu.

Hyperinsulinemia is associated with hypertension. Dysregulation of renal distal tubule sodium reabsorption may play a role. We evaluated the regulation of the epithelial sodium channel (ENaC) and the thiazide-sensitive Na-Cl cotransporter (NCC) during chronic hyperinsulinemia in rats and correlated these changes to blood pressure as determined by radiotelemetry. Male, Sprague-Dawley rats (~270 g) underwent one of the following 3 treatments for 4 weeks (n = 6/group): 1) control; 2) insulin-infused plus 20% dextrose in drinking water; or 3) glucose-drinking (20% dextrose in water). Mean arterial pressures were increased by insulin and glucose (mm Hg at 3 weeks): 98 ± 1 (control), 107 ± 2 (insulin), and 109 ± 3 (glucose), p < 0.01. Insulin (but not glucose) increased natriuretic response to benzamil (ENaC inhibitor) and hydrochlorothiazide (NCC inhibitor) on average by 125 and 60%, respectively, relative to control rats, suggesting increased activity of these reabsorptive pathways. Neither insulin nor glucose majorly affected the renal protein abundances of NCC or the ENaC subunits ({alpha}- {beta}- and {gamma}-) in kidney cortex, outer medulla, or inner medulla, as determined by immunoblotting. However, insulin and to some extent glucose, increased apical localization of these subunits in cortical collecting duct principal cells, as determined by immunoperoxidase labeling. In addition, insulin decreased cortical WNK4 ("with no lysine" kinase) abundance (by 16% relative to control) which may have increased NCC activity. Overall, insulin infusion increased blood pressure, and NCC and ENaC activity in rats. Increased apical targeting of ENaC and decreased WNK4 expression may be involved.




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