title: Metabolism-dependence of overdrive-induced hyperpolarization.
abstract: The mechanism by which fast drive ("overdrive") increases the maximum diastolic potential in cardiac Purkinje fibers was further analyzed by depressing metabolism in different ways. Both elecrical and mechanical events were recorded. It was found that, after an initial decline, contractile force increased during and after the overdrive. At the same time, the maximum diastolic potential gradually increased during and then declined after overdrive, as expected. Depression of metabolism by antimycin A, idodoacetate, low temperature and 2-deoxyglucose decreased or abolished the overdrive-induced hyperpolarization. These interventions affected the contractile force differently but did not prevent the increase in force during and after overdrive. The results suggest that during overdrive cellular calcium increases in the absence and presence of metabolic inhibition (as the contractile force increased), but the important factor in overdrive-induced hyperpolarization is an electrogenic sodium extrusion, rather than a calcium-induced increase in potassium conductance.
mesh_terms: D000818:Animals; D000963:Antimetabolites / Q000494:pharmacology*; D000968:Antimycin A / Q000494:pharmacology; D001831:Body Temperature / Q000187:drug effects; D002118:Calcium / Q000378:metabolism*; D003847:Deoxyglucose / Q000494:pharmacology; D004285:Dogs; D006329:Heart Conduction System / Q000502:physiology*; D007461:Iodoacetates / Q000494:pharmacology; D011690:Purkinje Fibers / Q000378:metabolism / Q000502:physiology*
chemical_list: D000963:Antimetabolites; D007461:Iodoacetates; D000968:Antimycin A; D003847:Deoxyglucose; D002118:Calcium