Transcriptional Regulation of Sodium Transport by Vasopressin in Renal Cells*

Abstract

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 vivo 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 × 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.