Journal of Biological Chemistry
Volume 276, Issue 50, 14 December 2001, Pages 47087-47093
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MEMBRANE TRANSPORT STRUCTURE FUNCTION AND BIOGENESIS
Short Term Effect of Aldosterone on Na,K-ATPase Cell Surface Expression in Kidney Collecting Duct Cells*

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Aldosterone controls extracellular volume and blood pressure by regulating Na+ reabsorption, in particular by epithelia of the distal nephron. A main regulatory site of this transcellular transport is the epithelial sodium channel (ENaC) that mediates luminal Na+ influx. The Na,K-ATPase (Na+ pump) that coordinately extrudes Na+across the basolateral membrane is known to be regulated by short term aldosterone as well. We now show that in the cortical collecting duct (CCD) from adrenalectomized rats, the increase in Na,K-ATPase activity (approximately 3-fold in 3 h), induced by a single aldosterone injection, can be fully accounted by the increase in Na,K-ATPase cell surface expression (+ 497 ± 35%). The short term aldosterone action was further investigated in cultured mouse collecting duct principal cells mpkCCDcl4. Within 2 h, maximal Na,K-ATPase function assessed by Na+ pump current (I p) measurements and Na,K-ATPase cell surface expression were increased by 20–50%. Aldosterone did not modify the Na+ dependence of the Na+ pumps and induced transcription- and translation-dependent actions on pump surface expression and current independently of ENaC-mediated Na+ influx. In summary, short term aldosterone directly increases the cell surface expression of pre-existing Na+pumps in kidney CCD target cells. Thus, aldosterone controls Na+ reabsorption in the short term not only by regulating the apical cell surface expression of ENaC (Loffing, J., Zecevic, M., Feraille, E., Kaissling, B., Asher, C., Rossier, B. C., Firestone, G. L., Pearce, D., and Verrey, F. (2001) Am. J. Physiol. 280, F675–F682) but also by coordinately acting on the basolateral cell surface expression of the Na,K-ATPase.

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Published, JBC Papers in Press, October 11, 2001, DOI 10.1074/jbc.M107165200

*

This work was supported by Swiss National Science Foundation Grants 31-59141.99 (to F. V.) and 31-50830.99 (to E. F.), by the Hartmann-Müller Stiftung in Zürich, and by the Carlos and Elsie de Reuter Foundation in Geneva.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

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These authors contributed equally to this work.