title: Surface expression of sodium channels and transporters in rat kidney: effects of dietary sodium.
abstract: The abundance of Na transport proteins in the luminal membrane of the rat kidney was assessed using in situ biotinylation and immunoblotting. When animals were fed an Na-deficient diet for 1 wk, the amounts of epithelial Na channel (ENaC) beta-subunit (beta-ENaC) and gamma-subunit (gamma-ENaC) and Na-Cl cotransporter (NCC) protein in the surface fraction increased relative to controls by 1.9-, 3.5-, and 1.5-fold, respectively. The amounts of the luminal Na/H exchanger (NHE3) and the luminal Na-K-2Cl cotransporter (NKCC2) did not change significantly. The increases in ENaC subunits were mimicked by administration of aldosterone for 1 wk, but the increase in NCC was not. When the animals were fed a high-Na (5% NaCl) diet for 1 wk, the surface expression of beta-ENaC increased by 50%, whereas that of the other membrane proteins did not change, relative to controls. The biochemical parameter most strongly affected by dietary Na was the abundance of the 65-kDa cleaved form of gamma-ENaC at the surface. This increased by 8.5-fold with Na depletion and decreased by 40% with Na loading. The overall 14-fold change reflected regulation of the total abundance of the subunit as well as the fraction of the subunit protein in the cleaved form. We conclude that cleavage of gamma-ENaC and its expression at the apical surface play a major role in the regulation of renal Na reabsorption.
authors.affiliation: Department of Physiology and Biophysics, Weill Medical College of Cornell University, New York, NY 10065, USA.
authors.forename: Gustavo
authors.initials: G
authors.lastname: Frindt
authors.forename: Lawrence G
authors.initials: LG
authors.lastname: Palmer
mesh_terms: D000818:Animals; D001710:Biotin / Q000378:metabolism; D002352:Carrier Proteins / Q000096:biosynthesis*; D004232:Diuretics / Q000494:pharmacology; D004591:Electrophoresis, Polyacrylamide Gel; D053503:Epithelial Sodium Channels / Q000096:biosynthesis / Q000235:genetics; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000172:deficiency; D015222:Sodium Channels / Q000096:biosynthesis*; D012982:Sodium, Dietary / Q000494:pharmacology*; D000074083:Sodium-Hydrogen Exchanger 3; D017923:Sodium-Hydrogen Exchangers / Q000096:biosynthesis / Q000235:genetics; D028021:Sodium-Potassium-Chloride Symporters / Q000096:biosynthesis / Q000235:genetics; D064466:Solute Carrier Family 12, Member 1; D049971:Thiazides / Q000494:pharmacology
chemical_list: D002352:Carrier Proteins; D004232:Diuretics; D053503:Epithelial Sodium Channels; C440894:Scnn1a protein, rat; C578716:Slc12a1 protein, rat; C000613387:Slc9a3 protein, rat; D015222:Sodium Channels; D012982:Sodium, Dietary; D000074083:Sodium-Hydrogen Exchanger 3; D017923:Sodium-Hydrogen Exchangers; D028021:Sodium-Potassium-Chloride Symporters; D064466:Solute Carrier Family 12, Member 1; D049971:Thiazides; D001710:Biotin; D012964:Sodium