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1 University of Aarhus, The Water and Salt Research Center, DK-8000 Aarhus C, Denmark; University of Aarhus, Institute of Anatomy, DK-8000 Aarhus C, Denmark
2 University of Aarhus, The Water and Salt Research Center, DK-8000 Aarhus C, Denmark; School of Medicine, Kyungpook National University, Department of Biochemistry and Cell Biology, Taegu, Korea, Republic of
3 University of Aarhus, The Water and Salt Research Center, DK-8000 Aarhus C, Denmark; University of Aarhus, Institute of Clinical Medicine, DK-8000 Aarhus C, Denmark
4 National Institutes of Health, National Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, Bethesda, Maryland, United States
* To whom correspondence should be addressed. E-mail: sn{at}ana.au.dk.
Aldosterone induces redistribution of 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 to untreated control rats. Co-treatment with spironolactone completely blocked the aldosterone-induced decrease in plasma K+. Immunoblotting and immunohistochemistry showed increased protein abundance of Na,K-ATPase 
1-subunit and NCC in the kidney cortex in response to aldosterone-infusion which 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 ENaC showed increased protein abundance in aldosterone-infused rats which 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 prevented neither ENaC trafficking, nor the upregulation of 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.
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