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.