Carbon dioxide, membrane potential and intracellular potassium activity in frog skeletal muscle.

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Abstract
The membrane potential of isolated frog muscle fibers was measured in absence and in presence of CO2, at constant external pH. At a normal external Cl concentration, CO2 (PCO2 [partial pressure] = 97 mmHg; pH = 7.0) applied for 10 min caused a highly variable depolarization, the average potential change being 8 mV after 5 min. The effect was reversible. In Cl-free solutions, CO2 (PCO2 = 97 mmHg; pH = 7.0) caused a biphasic depolarization of 20 mV after 5 min. The effect was fully reversible on CO2 removal. The same effect appeared at a lower partial pressure (PCO2 = 38 mmHg; pH 7.3) in the presence of tetrodotoxin (10-7 M). To investigate the cause of the CO2-induced depolarization, membrane potential and intracellular K activity .**GRAPHIC**. of surface muscle fibers were measured with voltage and ion-sensitive micro-electrodes. At a normal external Cl concentration, CO2(PCO2 .simeq. 97 mmHg; pH = 7.0) decreased .**GRAPHIC**. by 5 mM after 5 min. The same effect appeared at low external Cl concentration (11 mM). At high partial pressure (PCO2 .simeq. 588 mmHg; pH = 6.8), CO2 reduced .**GRAPHIC**. by 19 mM in 10 min. In long-term experiments performed over 4 h with a normal external Cl concentration, CO2 (PCO2 .simeq. 97 mmHg; pH 5.8 or 7) changed practically neither membrane potential, nor .**GRAPHIC**. Increasing the PCO2 when keeping the external pH constant causes an early depolarization of muscle. This effect is particularly marked in the absence of chloride. It can be explained partly, in surface muscle fibers, by a decrease of the intracellular K activity.