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J. Biol. Chem., Vol. 276, Issue 50, 47087-47093, December 14, 2001

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Short Term Effect of Aldosterone on Na,K-ATPase Cell Surface Expression in Kidney Collecting Duct Cells^*

Vanessa Summa^§, David Mordasini^§¶, Frank Roger^¶, Marcelle Bens, Pierre-Yves Martin^¶, Alain Vandewalle, François Verrey^**, and Eric Féraille^¶

From the  Institute of Physiology, University of Zürich, Zürich, CH-8057 Switzerland, the ^¶ Division of Nephrology and Department of Pathology, University of Geneva, CH-1211 Geneva, Switzerland, and  INSERM, Unité 478, Faculté de Médecine Xavier-Bichat, 75870 Paris Cedex 18, France

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 mpkCCD_cl4. 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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