Na+-H+ exchange at the apical membrane of Necturus gallbladder. Extracellular and intracellular pH studies.
The mechanism of luminal solution acidification was studied in Necturus gallbladder by measurement of mucosal solution and intracellular pH with glass electrodes. When the gallbladder was bathed by a Na-Ringer's solution it acidified the luminal side by a Na+-dependent, amiloride-inhibitable process. In the presence of ouabain, acidification was reduced but could be stimulated to a rate greater than that under control conditions by the imposition of an inwardly directed Na+ gradient. These results suggest that luminal acidification results from Na+-H+ exchange at the apical membrane and not by diffusion of metabolic CO2. Li+ can substitute for Na+ but K+, Rb+, Cs+, and tetramethylammonium (TMA+) cannot. The maximal rate of exchange was about five times greater for Na+ than for Li+. Intracellular pH (pHi) was measured with recessed-tip glass microelectrodes; with the tissue bathed in Na-Ringer's solution (pH 7.75), pHi was 7.51 +/- 0.04. After inhibition of Na+-H+ exchange by mucosal perfusion with amiloride (1 mM) or by complete Na+ replacement with TMA+, phi fell reversibly by 0.15 and 0.22 pH units, respectively. These results support the conclusion that Na+-H+ exchange at the apical membrane is the mechanism of luminal acidification and is involved in the maintenance of steady state pHi.
D000143:Acids / Q000378:metabolism; D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D001639:Bicarbonates / Q000378:metabolism; D005704:Gallbladder / Q000378:metabolism*; D006863:Hydrogen-Ion Concentration; D008094:Lithium / Q000494:pharmacology; D008564:Membrane Potentials; D009337:Necturus; D010042:Ouabain / Q000494:pharmacology; D012964:Sodium / Q000378:metabolism*
D000143:Acids; D001639:Bicarbonates; D010042:Ouabain; D000584:Amiloride; D008094:Lithium; D012964:Sodium