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

Abstract

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 (alpha, beta, and gamma) in rat kidney. Seven-day infusion of 1-deamino-[8-D-arginine]-vasopressin (dDAVP) to Brattleboro rats markedly increased whole kidney abundances of beta- and gamma-ENaC (to 238% and 288% of vehicle, respectively), whereas alpha-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 beta- and gamma- but no significant change in alpha-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.

Axial heterogeneity of vasopressin-receptor subtypes along the human and mouse collecting duct

“…At physiological concentrations of 10 Ϫ11 M, the antidiuretic action of vasopressin is mediated via V2 receptors coupled to adenylate cyclase, inducing PKA-mediated AQP2 phosphorylation and its translocation to the apical membrane of principal collecting duct cells (43). AVP not only induces water reabsorption in collecting ducts, but also modulates Na ϩ reabsorption (10,21,42) and K ϩ secretion (4,40).…”

Mild dehydration, vasopressin and the kidney: animal and human studies

“…This effect involves the activation of the amiloride-sensitive epithelial sodium channel (ENaC). It has been shown recently that vasopressin not only has an acute impact on ENaC-dependent sodium transport (Tomita et al, 1985;Verrey, 1994;Blot-Chabaud et al, 1996;Djelidi et al, 1997) but also has a delayed effect on the expression of b and gENaC subunits, in the kidney, by activating the V2 receptors (Ecelbarger et al, 2000;Nicco et al, 2001) (Figure 3). This effect is accompanied by a significant increase in sodium and water transport (Nicco et al, 2001) (Figure 4), suggesting associated changes in functional ENaC membrane proteins.…”

Transcriptome of a mouse kidney cortical collecting duct cell line: Effects of aldosterone and vasopressin

“…V2R-stimulated cell cAMP content triggers transepithelial sodium, chloride, and water reabsorption by a two-phase mechanism (3,12,13): (i) during a short-term, nongenomic phase, vasopressin rapidly increases the number of functional ENaC and the density of aquaporin-2 molecules in the apical membrane of principal cells; and (ii) during the late, genomic phase, vasopressin participates to the long-term regulation of renal sodium, chloride, and water reabsorption through the cAMP-dependent transcriptional activation of a gene network that includes aquaporin-2 (14, 15), Na,KATPase, ENaC, and the cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel (3,13). By analogy to aldosterone-dependent transcripts (AITs and ARTs), vasopressininduced and vasopressin-repressed transcripts are referred to as VITs and VRTs, respectively.…”