The prolongation of the action potential in mammalian ventricular muscle at rest. Is it due to intracellular calcium content changes.
The conventional microelectrode technique was used to investigate the effect of long periods of rest (greater than 10s) on the action potential duration of mammalian ventricular muscle. The action potential duration increased as the rest period increased. This prolongation of the action potential was the greatest and the slowest in rabbit ventricle, was smaller and more rapid in guinea-pig ventricle, and was practically absent in rat ventricle. The prolongation of the action potential at rest was suppressed with aminazine and strophanthin. Low sodium concentration, lanthanum ions, ruthenium red and acidosis failed to suppress the slow prolongation. It is concluded that the slow prolongation of the action potential at rest is related to changes in the intracellular calcium content induced by a mechanism different from Na/Ca exchange.
D000200:Action Potentials / Q000187:drug effects*; D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D002118:Calcium / Q000378:metabolism / Q000502:physiology*; D002746:Chlorpromazine / Q000494:pharmacology; D003864:Depression, Chemical; D004558:Electric Stimulation; D006168:Guinea Pigs; D066298:In Vitro Techniques; D010210:Papillary Muscles / Q000502:physiology*; D011817:Rabbits; D051381:Rats; D012146:Rest; D012964:Sodium / Q000378:metabolism; D013328:Strophanthins / Q000494:pharmacology; D013997:Time Factors; D016276:Ventricular Function
D013328:Strophanthins; D012964:Sodium; D002118:Calcium; D002746:Chlorpromazine