Chloride dependence of the HCO3 exit step in urinary acidification by the turtle bladder

Am J Physiol. 1983 Nov;245(5 Pt 1):F564-8. doi: 10.1152/ajprenal.1983.245.5.F564.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Bicarbonates / urine*
  • Calcium Gluconate / pharmacology
  • Chlorides / urine*
  • Hydrogen-Ion Concentration
  • Ouabain / pharmacology
  • Sulfuric Acid Esters / pharmacology
  • Turtles / physiology*
  • Urinary Bladder / drug effects
  • Urinary Bladder / physiology*
  • Urine

Substances

  • Bicarbonates
  • Chlorides
  • Sulfuric Acid Esters
  • Ouabain
  • methyl sulfate
  • Calcium Gluconate