Vasopressin-mediated regulation of epithelial sodium channel abundance in rat kidney

Sodium transport is increased by vasopressin in the cortical collecting duc ts of rats and rabbits. Here we investigate, by quantitative immunoblotting , the effects of vasopressin on abundances of the epithelial sodium channel (ENaC) subunits (alpha, beta, and gamma) in rat kidney. Seven-day infusion of 1-deamino-[8-D-arginine]-vasopressin (dDAVP) to Brattleboro rats marked ly increased whole kidney abundances of band gamma-ENaC (to 238% and 288% o f vehicle, respectively), whereas alpha-ENaC was more modestly, yet signifi cantly, increased (to 142% of vehicle). Similarly, 7-day water restriction in Sprague-Dawley rats resulted in significantly increased abundances of be ta- and gamma- but no significant change in alpha-ENaC. Acute administratio n of dDAVP (2 nmol) to Brattleboro rats resulted in modest, but significant , increases in abundance for all ENaC subunits, within 1 h. In conclusion, all three subunits of ENaC are upregulated by vasopressin with temporal and regional differences. These changes are too slow to play a major role in t he short-term action of vasopressin to stimulate sodium reabsorption in the collecting duct. Long-term increases in ENaC abundance should add to the s hort-term regulatory mechanisms (undefined in this study) to enhance sodium transport in the renal collecting duct.