Stimulation of chloride transport by HCO3-CO2 in rabbit cortical collecting tubule

K. Tago, V. L. Schuster, J. B. Stokes

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38 Scopus citations


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 K(Cl), 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 K(Cl) 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 K(Cl). Acetazolamide addition in HEPES-buffered solutions also lowered K(Cl); K(Cl) 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 K(Cl) and did so to a greater degree in tubules from HCO3-loaded rabbits. Most of this effect of HCO3-CO2 addition on K(Cl) 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.

Original languageEnglish (US)
Pages (from-to)20/1
JournalAmerican Journal of Physiology - Renal Fluid and Electrolyte Physiology
Issue number1
StatePublished - Jan 1 1986
Externally publishedYes

ASJC Scopus subject areas

  • Physiology


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