Effects of acid‐base changes on excitation‐‐contraction coupling in guinea‐pig and rabbit cardiac ventricular muscle.

Abstract

Respiratory and metabolic acid-base changes caused similar steady-state changes in the contractility of cardiac ventricular muscle, but the rate of response was more rapid with the former intervention. Variations in extracellular PCO2 [partial pressure of CO2] and [HCO3-] at constant pH caused only a transient change in contractility. An intracellular pH change can describe the above events. The changes in contractility caused by extracellular acid-base changes could be explained by competition between Ca2+ and H+ ions for a single process. Assuming an electroneutral scheme whereby 1 extracellular Ca2+ ion or 2 intracellular H+ ions compete for a binding site, the interior of ventricular cells must be better buffered than the extracellular fluid. H+ ions evoked a release of Ca2+ ions from a mitochondrial suspension with a time course similar to the partial recovery of tension observed during a respiratory acidosis. Respiratory and metabolic acidoses depressed the action potential plateau and prolonged repolarization. The resting potential and the maximum rate of depolarization were unaffected by the above acid-base changes. An acidosis depressed Ca2+ influx through the slow inward channel by an amount sufficient to account for the observed contractility changes. Between pH 7.6 and 6.6 the major physiological effect of an acidosis is to depress the slow inward current as a result of an intracellular pH change.