AJP - Renal Physiology, Vol 245, Issue 5 564-F568, Copyright © 1983 by American Physiological Society
Chloride dependence of the HCO3 exit step in urinary acidification by the turtle bladder
J. L. Fischer, R. F. Husted and P. R. Steinmetz
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.
