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Altered expression of epithelial sodium channel in rats with bilateral or unilateral ureteral obstruction

¹The Water and Salt Research Center, ²Institute of Clinical Medicine, and ³Department of Cell Biology, Institute of Anatomy, University of Aarhus, Aarhus C, Denmark; ⁴Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland; and ⁵Department of Clinical Physiology, Aarhus University Hospital-Skejby, Aarhus N, Denmark

Submitted 15 September 2006 ; accepted in final form 23 April 2007

The roles of epithelial sodium channel (ENaC) subunits (, , and ) in the impaired renal reabsorption of sodium and water were examined in rat models with bilateral (BUO) or unilateral ureteral obstruction (UUO) for 24 h or with BUO followed by release of obstruction and 3 days of observation (BUO-3dR). In BUO rats, plasma osmolality was increased dramatically, whereas plasma sodium concentration was decreased. Immunoblotting revealed a significantly decreased expression of -ENaC (57 ± 7%), -ENaC (19 ± 5%), and -ENaC (51 ± 10%) as well as 11-hydroxysteroid dehydrogenase type 2 (11-HSD2) in the cortex and outer medulla (C+OM) compared with sham-operated controls. This was confirmed by immunohistochemistry. BUO-3dR was associated with polyuria and impaired renal sodium handling. The protein abundance and the apical labeling of -ENaC were significantly increased, whereas - and -ENaC as well as 11-HSD2 expression remained decreased. In UUO rats, expression of - and -ENaC and 11-HSD2 decreased in the C+OM in the obstructed kidney. In contrast, the abundance and the apical labeling of -ENaC in the nonobstructed kidneys were markedly increased, suggesting compensatory upregulation in this kidney. In conclusion, -, -, and -ENaC expression levels are downregulated in the obstructed kidney. The expression and apical labeling of -ENaC were increased in BUO-3dR rats and in the nonobstructed kidneys from UUO rats. These results suggest that altered expression of -, -, and -ENaC may contribute to impaired renal sodium and water handling in response to ureteral obstruction.

collecting duct; distal convoluted tube; sodium transport; sodium reabsorption; obstructive nephropathy

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