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Articles in PresS, published online ahead of print June 26, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00015.2002
Submitted on January 11, 2002
Accepted on June 23, 2002
1 National Heart, Lung and Blood Institute, National Institute of Health, Bethesda, MD, USA; The Water and Salt Reacher Center, University of Aarhus, Aarhus, Denmark
2 The Water and Salt Reacher Center, University of Aarhus, Aarhus, Denmark
3 National Heart, Lung and Blood Institute, National Institute of Health, Bethesda, MD, USA
* To whom correspondence should be addressed. E-mail: knep{at}helix.nih.gov.
Renal tubule profiling studies were carried out to investigate the long-term effects of administration of spironolactone, a mineralocorticoid receptor antagonist, on abundances of the major Na transporter and Na channel proteins along the rat renal tubule. Oral administration of spironolactone for 7 days to NaCl-restricted rats did not significantly alter abundances of Na transporters expressed proximal to the macula densa, while substantially decreasing the abundances of the thiazide-sensitive Na-Cl cotransporter (NCC), the 
subunit of the amiloride-sensitive Na channel (ENaC), and the 70 kDa form of the 
subunit of ENaC. A dependency of NCC expression on aldosterone was confirmed by showing increased NCC expression in response to aldosterone infusion in adrenalectomized rats. Immunoperoxidase labeling of ENaC in renal cortex confirmed that dietary NaCl restriction causes a redistribution of ENaC to the apical domain of connecting tubule cells and showed that high-dose spironolactone administration does not block this apical redistribution. In contrast, spironolactone completely blocked the increase in -ENaC abundance in response to dietary NaCl restriction. We conclude that the protein abundances of NCC, -ENaC and the 70kDa form of -ENaC are regulated via the classical mineralocorticoid receptor, but that the subcellular redistribution of ENaC in response to dietary NaCl restriction is not prevented by blockade of the mineralocorticoid receptor.
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