A Dynamic Model of the Cardiac Ventricular Action Potential: I. Simulations of Ionic Currents and Concentration Changes

A mathematical model of the cardiac ventricular action potential is presented. In our previous work, the membrane Na current and K currents were formulated. The present article focuses on processes that regulate intracellular Ca and depend on its concentration. The model presented here for the mamma...

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Bibliographic Details
Published in:Circulation research 1994-06, Vol.74 (6), p.1071-1096
Main Authors: Luo, Ching-Hsing, Rudy, Yoram
Format: Article
Language:English
Subjects:
Action Potentials
Animals
Calcium - metabolism
Calcium Channels - physiology
Carrier Proteins - physiology
Guinea Pigs
Heart - physiology
Ion Channels - physiology
Models, Biological
Potassium Channels - physiology
Sodium-Calcium Exchanger
Sodium-Potassium-Exchanging ATPase
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Summary:A mathematical model of the cardiac ventricular action potential is presented. In our previous work, the membrane Na current and K currents were formulated. The present article focuses on processes that regulate intracellular Ca and depend on its concentration. The model presented here for the mammalian ventricular action potential is based mostly on the guinea pig ventricular cell. However, it provides the framework for modeling other types of ventricular cells with appropriate modifications made to account for species differences. The following processes are formulatedCa current through the L-type channel (ICa), the Na-Ca exchanger, Ca release and uptake by the sarcoplasmic reticu-lum (SR), buffering of Ca in the SR and in the myoplasm, a Ca pump in the sarcolemma, the Na-K pump, and a nonspecific Ca-activated membrane current. Activation of ICa is an order of magnitude faster than in previous models. Inactivation of ICa depends on both the membrane voltage and [Ca],. SR is divided into two subcompartments, a network SR (NSR) and a junctional SR (JSR). Functionally, Ca enters the NSR and translocates to the JSR following a monoexponential function. Release of Ca occurs at JSR and can be triggered by two different mechanisms, Ca-induced Ca release and spontaneous release. The model provides the basis for the study of arrhythmogenic activity of the single myocyte including afterdepolarizations and triggered activity. It can simulate cellular responses under different degrees of Ca overload. Such simulations are presented in our accompanying article in this issue of Circulation Research.
ISSN:0009-7330
1524-4571
DOI:10.1161/01.res.74.6.1071