Bicarbonate/chloride antiport in vero cells: II. Mechanisms for bicarbonate‐dependent regulation of intracellular pH

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Abstract
The rates of bicarbonate‐dependent uptake and efflux of 22Na+ in Vero cells were studied and compared with the uptake and efflux of 36Cl−. Both processes were strongly inhibited by DIDS. Whereas the transport of chloride increased approximately ten‐fold when the internal pH was increased over a narrow range around neutrality, the uptake of Na+ was much less affected by changes in pH. The bicarbonate‐linked uptake of 22Na+ was dependent on internal Cl− but not on internal Na+. At a constant external concentration of HCO−3, the amount of 22Na+ associated with the cells increased when the internal concentration of HCO−3 decreased and vice versa, which is compatible with the possibility that the ion pair NaCO−3 is the transported species and that the transport is symmetric across the membrane. Bicarbonate inhibited the uptake of 36Cl− both in the absence and presence of Na+. At alkaline internal pH, HCO−3 stimulated the efflux of 36Cl− from preloaded cells, while at acidic internal pH both Na+ and HCO−3 were required to induce 36Cl− efflux. We propose a model for how bicarbonate‐dependent regulation of the internal pH may occur. This model implies the existence of two bicarbonate transport mechanisms that, under physiological conditions, transport OH−‐ equivalents in opposite directions across the plasma membrane.