Anion channels contribute to the regulation of intracellular pH in human platelets

The presence of extracellular bicarbonate potentiated platelet intracellular pH rises induced by thrombin. The effect was most remarkable in sodium-depleted buffers. This effect of bicarbonate was dose-dependent and was inhibited by anion channel blockers. Bicarbonate also potentiated the pHi recovery after acid loading, but had no effect on alkali loading. It was suggested that anion exchange, most probably that of bicarbonate/chloride, contributes to the regulation of intracellular pH in human platelets.