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Increased collecting duct urea transporter expression in Dahl salt-sensitive rats

¹Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and BIood Institute, National Institutes of Health, Bethesda, Maryland 20892; and ²Department of Internal Medicine, University of Iowa, and Veterans Affairs Medical Center, Iowa City, Iowa 52242

Submitted 24 February 2003 ; accepted in final form 20 April 2003

Because abnormalities of inner medullary function have been proposed in Dahl salt-sensitive (DS) rats vs. salt-resistant (DR) rats, we performed transporter profiling by semiquantitative immunoblotting to determine whether specific solute transporter abundances are altered in inner medullas of DS rats vs. DR rats. Although none of the expressed Na transporters were upregulated in the inner medullas of DS rats compared with DR rats, there were marked increases in the protein abundances of the collecting duct urea transporters UT-A1 (to 212% of DR) and UT-A3 (to 223% of DR). These differences were confirmed by immunocytochemistry. Quantitative real-time RT-PCR showed higher mRNA abundance in DS rats for both UT-A1 (to 256% of DR) and UT-A3 (to 210% of DR). In isolated, perfused inner medullary collecting ducts, urea permeability was significantly greater in DS rats. Because both UT-A1 and UT-A3 are transcriptionally regulated by glucocorticoids, we measured both plasma corticosterone levels and inner medullary 11-hydroxysteroid dehydrogenase type 2 (11-HSD2) abundances. Although the plasma corticosterone concentrations were not different between DS and DR rats, immunoblotting and immunocytochemistry revealed a marked elevation of 11-HSD2 abundance in DS rats. Consistent with the view that an elevated 11-HSD2 level is responsible for increased urea transporter expression in the inner medullary collecting duct, administration of the 11-HSD2 inhibitor carbenoxolone to DS rats decreased the abundances of UT-A1 and UT-A3 to levels similar to those seen in DR rats.

UT-A; sodium-potassium-adenosine 5'-triphosphatase; 11-hydoxysteroid dehydrogenase; glucocorticoid

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