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Volume 272, Number 52, Issue of December 26, 1997 pp. 32919-32924

Transcriptional Regulation of Sodium Transport by Vasopressin in Renal Cells

(Received for publication, April 25, 1997, and in revised form, September 5, 1997)

Sabri Djelidi , Michel Fay , Françoise Cluzeaud , Brigitte Escoubet ^§ , Emmanuel Eugene , Claudia Capurro , Jean-Pierre Bonvalet , Nicolette Farman and Marcel Blot-Chabaud

From INSERM  U246 and ^§ U426, Institut Fédératif de Recherches "Cellules Epithéliales," Faculté de Médecine Xavier Bichat, 16, rue Henri Huchard, 75870 Paris Cedex 18, France

We have examined whether arginine vasopressin (AVP) can induce a long-term modulation of transepithelial ion transport in addition to its well known short-term effect. In the RCCD₁ rat cortical collecting duct cell line, an increase in both short-circuit current and ²²Na transport was observed after several hours of 10⁸ M AVP treatment (a concentration above the in vivo physiological range). This delayed effect was partially prevented by apical addition of 10⁵ M amiloride and was blocked by 10⁶ M actinomycin D and 2 × 10⁶ M cycloheximide. The amounts of mRNA encoding the ₁ (not ₁) subunit of Na⁺/K⁺-ATPase and the  and  (not ) subunits of the amiloride-sensitive epithelial Na⁺ channel were significantly increased by AVP treatment. The increase in mRNA was blocked by actinomycin D, not by amiloride, suggesting a Na⁺-independent increase in the rate of transcription of these subunits. The translation rates of the ₁ subunit of Na⁺/K⁺-ATPase and the  and  subunits of the rat epithelial sodium channel increased significantly, whereas the translation rates of the other subunits remained unchanged. Finally, the number of Na⁺ channels present in the apical membrane of the cells increased, as demonstrated by enhanced specific [³H]phenamil binding.

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