Chloride dependence of the HCO3 exit step in urinary acidification by the turtle bladder.
To characterize the efflux of HCO-3 across the basolateral membrane of the H+-secreting cells of the turtle bladder, we examined the effect of substitution of gluconate or methyl sulfate for Cl- on the rate of acidification (JH). JH was measured as the short-circuit current in bladders in which Na+ transport was abolished with 10(-4) M ouabain. In hemibladders bathed in normal Ringer solution (Cl- = 122 mM) JH was 44.9 microA. Substitution of the Cl- resulted in a marked reduction in JH (12.5 microA with gluconate and 7.5 microA with methyl sulfate). Addition of Cl- to the mucosal surface had no effect on JH. In contrast, serosal addition of Cl- restored JH to control. The apparent Km for Cl- in gluconate Ringer was 0.13 mM. Serosal furosemide (1 mM) inhibited JH by 55% in Cl- Ringer. We conclude that HCO-3 exit across the basolateral membrane of the H+-secreting cell occurs via a Cl-HCO3 exchanger that has a high affinity for chloride.
D000818:Animals; D001639:Bicarbonates / Q000652:urine*; D002125:Calcium Gluconate / Q000494:pharmacology; D002712:Chlorides / Q000652:urine*; D006863:Hydrogen-Ion Concentration; D010042:Ouabain / Q000494:pharmacology; D013463:Sulfuric Acid Esters / Q000494:pharmacology; D014426:Turtles / Q000502:physiology*; D001743:Urinary Bladder / Q000187:drug effects / Q000502:physiology*; D014556:Urine
D001639:Bicarbonates; D002712:Chlorides; D013463:Sulfuric Acid Esters; D010042:Ouabain; C033522:methyl sulfate; D002125:Calcium Gluconate