AJP - Renal Physiology, Vol 251, Issue 1 49-F56, Copyright © 1986 by American Physiological Society
Stimulation of chloride transport by HCO3-CO2 in rabbit cortical collecting tubule
K. Tago, V. L. Schuster and J. B. Stokes
We examined both the role of HCO3-CO2 in Cl transport as well as the effect
of in vivo acid-base status on Cl transport by the rabbit cortical
collecting tubule. The lumen-to-bath 36Cl tracer flux, expressed as the
rate coefficient KCl, was measured in either HEPES-buffered (CO2-free) or
HCO3-CO2-containing solutions. Amiloride was added to the perfusate to
minimize the transepithelial voltage and thus the electrical driving force
for Cl diffusion. Because KCl fell spontaneously with time in HCO3-CO2
solutions in the absence but not the presence of cAMP, we used cAMP
throughout to avoid time-dependent changes. Acute in vitro removal of bath
HCO3-CO2 reduced KCl. Acetazolamide addition in HEPES-buffered solutions
also lowered KCl; KCl could be restored to control values by adding
exogenous HCO3-CO2 in the presence of acetazolamide. In vivo acid-base
effects on Cl transport were determined by dissecting tubules from either
NaHCO3-loaded or NH4Cl-loaded rabbits. Tubules from HCO3-loaded rabbits had
higher rates of Cl self exchange. Acute in vitro addition of bath HCO3-CO2
increased KCl and did so to a greater degree in tubules from HCO3-loaded
rabbits. Most of this effect of HCO3-CO2 addition on KCl could not be
accounted for by Cl-HCO3 exchange; rather, it appeared due to stimulation
of Cl self exchange. The data are consistent with 36Cl transport occurring
via Cl-HCO3 exchange as well as Cl self exchange. Both processes are
acutely stimulated by HCO3 and/or Co2, and both are chronically regulated
by in vivo acid-base status.
