Article,

A dynamic model of the cardiac ventricular action potential. II. Afterdepolarizations, triggered activity, and potentiation.

, and .
Circ. Res., 74 (6): 1097--1113 (June 1994)

Abstract

The action potential model presented in our accompanying article in this journal is used to investigate phenomena that involve dynamic changes of Ca$^2+$i, as described below. Delayed afterdepolarizations (DADs) are induced by spontaneous Ca$^2+$ release from the sarcoplasmic reticulum (SR), which, in turn, activates both the Na$^+$-Ca$^2+$ 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 Ca$^2+$ overload. Early afterdepolarizations (EADs) can be categorized into two types: (1) plateau EADs, resulting from a secondary activation of the L-type Ca$^2+$ current during the plateau of an action potential, and (2) phase-3 EADs, resulting from activation of INaCa and Ins(Ca) by increased Ca$^2+$i due to spontaneous Ca$^2+$ release from the SR during the late repolarization phase. Spontaneous rhythmic activity and triggered activity are caused by spontaneous Ca$^2+$ release from the SR under conditions of Ca$^2+$ overload. Postextrasystolic potentiation reflects the time delay associated with translocation of Ca$^2+$ from network SR to junctional SR. The cell is paced at high frequencies to investigate the long-term effects on the intracellular ionic concentrations.

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