title: A dynamic model of the cardiac ventricular action potential. II. Afterdepolarizations, triggered activity, and potentiation.
abstract: The action potential model presented in our accompanying article in this journal is used to investigate phenomena that involve dynamic changes of [Ca2+]i, as described below. Delayed afterdepolarizations (DADs) are induced by spontaneous Ca2+ release from the sarcoplasmic reticulum (SR), which, in turn, activates both the Na(+)-Ca2+ exchanger (INaCa) and a nonspecific Ca(2+)-activated current (Ins(Ca)). The relative contributions of INaCa and of Ins(Ca) to the generation of DADs are different under different degrees of Ca2+ overload. Early afterdepolarizations (EADs) can be categorized into two types: (1) plateau EADs, resulting from a secondary activation of the L-type Ca2+ current during the plateau of an action potential, and (2) phase-3 EADs, resulting from activation of INaCa and Ins(Ca) by increased [Ca2+]i due to spontaneous Ca2+ release from the SR during the late repolarization phase. Spontaneous rhythmic activity and triggered activity are caused by spontaneous Ca2+ release from the SR under conditions of Ca2+ overload. Postextrasystolic potentiation reflects the time delay associated with translocation of Ca2+ from network SR to junctional SR. The cell is paced at high frequencies to investigate the long-term effects on the intracellular ionic concentrations.
authors.affiliation: Department of Biomedical Engineering, Case Western Reserve University, Cleveland, OH 44106-7207.
authors.forename: C H
authors.initials: CH
authors.lastname: Luo
authors.forename: Y
authors.initials: Y
authors.lastname: Rudy
mesh_terms: D000200:Action Potentials; D000818:Animals; D002118:Calcium / Q000378:metabolism; D006168:Guinea Pigs; D006321:Heart / Q000502:physiology*; D007473:Ion Channels / Q000502:physiology; D008954:Models, Biological
chemical_list: D007473:Ion Channels; D002118:Calcium