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1 Division of Endocrinology, Georgetown University, Washington, District of Columbia 20007; 2 Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892
Sodium transport is increased
by vasopressin in the cortical collecting ducts of rats and
rabbits. Here we investigate, by quantitative immunoblotting, the
effects of vasopressin on abundances of the epithelial sodium channel
(ENaC) subunits (
, 
, and 
) in rat kidney. Seven-day infusion
of 1-deamino-[8-D-arginine]-vasopressin (dDAVP) to
Brattleboro rats markedly increased whole kidney abundances of - and
-ENaC (to 238% and 288% of vehicle, respectively), whereas
-ENaC was more modestly, yet significantly, increased (to
142% of vehicle). Similarly, 7-day water restriction in Sprague-Dawley rats resulted in significantly increased abundances of - and -
but no significant change in -ENaC. Acute administration 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 the short-term action of vasopressin to stimulate
sodium reabsorption in the collecting duct. Long-term increases in ENaC
abundance should add to the short-term regulatory mechanisms (undefined
in this study) to enhance sodium transport in the renal collecting duct.
immunoblotting; sodium transporters; collecting duct; Brattleboro rat; aldosterone
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