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Extracellular Ca2+ is obligatory for ouabain‐induced potentiation of cardiac basal energy expenditure

1. The method of action of cardiac glycosides is commonly explained by the ‘pump‐inhibition hypothesis’: inhibition of the Na+/K+‐ATPase allows [Na+]i to rise, eventually reversing Na+/Ca2+ exchange. The resulting influx of Ca2+o increases [Ca2+]i, thereby activating intracellular Ca2+‐dependent ATPases and, hence, energy demand. This sequence has been presumed to occur during diastole as well as systole. However, it has been reported that dihydro‐ouabain‐induced potentiation of heat production by quiescent ventricular trabeculae persists in the absence of Ca2+o. This implies that the pump‐inhibition hypothesis is inapplicable during diastole.