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Am J Physiol Renal Physiol 292: F382-F394, 2007. First published August 15, 2006; doi:10.1152/ajprenal.00212.2005
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Maintained ENaC trafficking in aldosterone-infused rats during mineralocorticoid and glucocorticoid receptor blockade

Jakob Nielsen,1,2 Tae-Hwan Kwon,1,3 Jørgen Frøkiær,1,4 Mark A. Knepper,5 and Søren Nielsen1,2

1The Water and Salt Research Center, University of Aarhus, Aarhus; 2Institute of Anatomy, University of Aarhus, Aarhus; 4Institute of Clinical Medicine, University of Aarhus, Aarhus, Denmark; 3Department of Biochemistry and Cell Biology, School of Medicine, Kyungpook National University, Taegu, Korea; and 5Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland

Submitted 20 May 2005 ; accepted in final form 9 August 2006

Aldosterone induces redistribution of epithelial sodium channel (ENaC) to the apical plasma membrane from intracellular vesicles in renal connecting tubule (CNT) and cortical collecting duct (CCD). The role of the classical mineralocorticoid receptor (MR) in ENaC trafficking is still debated. We examined whether the MR antagonist spironolactone affects ENaC regulation in the kidney cortex of aldosterone-infused rats. Aldosterone infusion for 7 days resulted in a plasma aldosterone concentration in the high physiological range (3 to 4 nM). Aldosterone infusion decreased plasma K+ concentration compared with untreated control rats. Cotreatment with spironolactone completely blocked the aldosterone-induced decrease in plasma K+. Immunoblotting and immunohistochemistry showed increased protein abundance of Na-K-ATPase {alpha}1-subunit and NCC in the kidney cortex, in response to aldosterone infusion that was blocked by spironolactone. In contrast, aldosterone-induced redistribution of ENaC subunits from the cytoplasm to the apical plasma membrane domain in CNT and CCD was unaffected by spironolactone. Immunoblotting of {alpha}ENaC showed increased protein abundance in aldosterone-infused rats that was not blocked by spironolactone treatment. To exclude possible glucocorticoid receptor (GR)-mediated effects of aldosterone, we treated aldosterone-infused rats with both spironolactone and the GR antagonist RU486. Combined MR and GR blockade prevented neither ENaC trafficking nor the upregulation of {alpha}ENaC protein abundance in aldosterone-infused rats. We provide new evidence for ENaC trafficking occurring independent of MR and GR activation in aldosterone-infused rats.

epithelial sodium channel; mineralocorticoid receptor


Address for reprint requests and other correspondence: S. Nielsen, The Water and Salt Research Center, Institute of Anatomy (Bldg. 233), Univ. of Aarhus, DK-8000 Aarhus, Denmark (e-mail: sn{at}ana.au.dk)




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