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- Title
Mechanism of Control of Na,K-ATPase in Principal Cells of the Mammalian Collecting Duct.
- Authors
FÉRAILLE, ERIC; MORDASINI, DAVID; GONIN, SANDRINE; DESCHÊNES, GEORGES; VINCIGUERRA, MANLIO; DOUCET, ALAIN; VANDEWALLE, ALAIN; SUMMA, VANESSA; VERREY, FRANÇOIS; MARTIN, PIERRE-YVES
- Abstract
A bstract: The collecting duct is the site of final Na reabsorption according to Na balance requirements. Using isolated rat cortical collecting ducts (CCD) and mpkCCDcl4 cells, a mouse cortical collecting duct cell line, we have studied the physiological control of Na,K-ATPase, the key enzyme that energizes Na reabsorption. Aldosterone, a major regulator of Na transport by the collecting duct, stimulates Na,K-ATPase activity through both recruitment of intracellular pumps and increased total amounts of Na pump subunits. This effect is observed after a lag time of 1 hour and is independent of Na entry through ENaC, but requires de novo transcription and translation. Vasopressin and cAMP, its second messenger, stimulate Na,K-ATPase activity within minutes through translocation of Na pumps from a brefeldin A-sensitive intracellular pool to the plasma membrane. Dysregulation of collecting duct Na,K-ATPase activity is at least in part responsible of the Na retention observed in nephritic syndrome. In this setting, Na,K-ATPase activity and subunit synthesis are specifically increased in CCD. In conclusion, aldosterone, vasopressin, and intracellular Na control the cell surface expression of Na,K-ATPase and translocation from intracellular stores is a major mechanism of regulation of Na,K-ATPase activity in collecting duct principal cells.
- Publication
Annals of the New York Academy of Sciences, 2003, Vol 986, Issue 1, p570
- ISSN
0077-8923
- Publication type
Article
- DOI
10.1111/j.1749-6632.2003.tb07255.x