A DYNAMIC-MODEL OF THE CARDIAC VENTRICULAR ACTION-POTENTIAL .2. AFTERDEPOLARIZATIONS, TRIGGERED ACTIVITY, AND POTENTIATION

Authors
Citation
Ch. Luo et Y. Rudy, A DYNAMIC-MODEL OF THE CARDIAC VENTRICULAR ACTION-POTENTIAL .2. AFTERDEPOLARIZATIONS, TRIGGERED ACTIVITY, AND POTENTIATION, Circulation research, 74(6), 1994, pp. 1097-1113
Citations number
32
Categorie Soggetti
Hematology,"Cardiac & Cardiovascular System
Journal title
ISSN journal
00097330
Volume
74
Issue
6
Year of publication
1994
Pages
1097 - 1113
Database
ISI
SICI code
0009-7330(1994)74:6<1097:ADOTCV>2.0.ZU;2-N
Abstract
The action potential model presented in our accompanying article in th is journal is used to investigate phenomena that involve dynamic chang es of [Ca2+](i), as described below. Delayed afterdepolarizations (DAD s) are induced by spontaneous Ca2+ release from the sarcoplasmic retic ulum (SR), which, in turn, activates both the Na+-Ca2+ exchanger (I-Na Ca) and a nonspecific Ca2+-activated current (I-ns(Ca)). The relative contributions of I-NaCa and of I-ns(Ca) to the generation of DADs are different under different degrees of Ca2+ overload. Early afterdepolar izations (EADs) can be categorized into two types: (1) plateau EADs, r esulting from a secondary activation of the L-type Ca2+ current during the plateau of an action potential, and (2) phase-3 EADs, resulting f rom activation of I-NaCa and I-ns(Ca) by increased [Ca2+](i) due to sp ontaneous Ca2+ release from the SR during the late repolarization phas e. 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 wi th 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.