Transcriptional Regulation of Sodium Transport by Vasopressin in Renal Cells

DJELIDI, SABRI; FAY, MICHEL; CLUZEAUD, FRANÇOISE; ESCOUBET, BRIGITTE; EUGENE, EMMANUEL; CAPURRO, CLAUDIA; BONVALET, JEAN-PIERRE; FARMAN, NICOLETTE; BLOT-CHABAUD, MARCEL

JOURNAL OF BIOLOGICAL CHEMISTRY

AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC

Año: 1997 vol. 272 p. 32919 - 32924

0021-9258

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 10-8 M AVP treatment (a concentration above the in vive physiological range). This delayed effect was partially prevented by apical addition of 10-5 M amiloride and was blocked by 10-6 M actinomycin D and 2 x 10-6 M cycloheximide. The amounts of mRNA encoding the α1 (not β1) subunit of Na+/K+-ATPase and the β and γ (not α) 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 α1 subunit of Na+/K+-ATPase and the β and γ 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.