Abstract
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$^2+$ 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 formulated: Ca$^2+$
current through the L-type channel (ICa), the Na$^+$-Ca$^2+$
exchanger, Ca$^2+$ release and uptake by the sarcoplasmic reticulum
(SR), buffering of Ca$^2+$ in the SR and in the myoplasm, a Ca$^2+$
pump in the sarcolemma, the Na$^+$-K$^+$ pump, and a nonspecific
Ca$^2+$-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$^2+$i. SR is divided
into two subcompartments, a network SR (NSR) and a junctional SR
(JSR). Functionally, Ca$^2+$ enters the NSR and translocates
to the JSR following a monoexponential function. Release of Ca$^2+$
occurs at JSR and can be triggered by two different mechanisms,
Ca$^2+$-induced Ca$^2+$ 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$^2+$ overload. Such simulations are presented in our accompanying
article in this issue of Circulation Research.
- 7514509
- action
- animals,
- atpase,
- biological,
- calcium
- calcium,
- carrier
- channels,
- exchanger,
- gov't,
- guinea
- heart,
- ion
- models,
- non-u.s.
- p.h.s.,
- pigs,
- potassium
- potentials,
- proteins,
- research
- sodium-calcium
- support,
- u.s.
- {n}a$^{+}$-{k}$^{+}$-exchanging
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