Chloride–Hydroxyl Exchange in the Guinea-pig Ventricular Myocyte: No Role for Bicarbonate

Reduction of extracellular pH (pHo) leads to a fall of intracellular pH (pHi) in the guinea-pig ventricular myocyte. In nominally CO2/HCO3−-free conditions, this has been attributed to stimulation of OH−ion efflux on a novel Cl−–OH−exchange carrier in the sarcolemma. In the present work, we have tested for the possible participation of bicarbonate ions. Residual bicarbonate levels may occur through hydration of CO2arising either from cellular metabolism or from the atmosphere. The pHiwas measured by using the intracellular pH-fluorophore, carboxy SNARF-1 (AM-loaded). Possible sources of CO2were eliminated by adding the aerobic inhibitors, cyanide or rotenone, and by equilibrating the superfusates flowing over the myocyte with a CO2-free, 100% N2atmosphere. The fall of pHiupon reducing pHo(to 6.4) persisted after complete CO2-removal. This indicates that, in nominally CO2-free conditions, residual HCO3−transport on a Cl−–HCO3−exchanger cannot account for the pHo-dependence of pHi, and supports the hypothesis for a Cl−-OH−exchanger (or, alternatively, an H+–Cl−co-influx mechanism).