Excitation-contraction coupling in an integrative heart cell model (Greenstein et al 2006)

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"... In this study, we generalize a recently developed analytical approach for deriving simplified mechanistic models of CICR (Ca(2+)-induced Ca(2+) release) to formulate an integrative model of the canine cardiac myocyte which is computationally efficient. The resulting model faithfully reproduces experimentally measured properties of EC (excitation-contraction) coupling and whole cell phenomena. The model is used to study the role of local redundancy in L-type Ca(2+) channel gating and the role of dyad configuration on EC coupling. Simulations suggest that the characteristic steep rise in EC coupling gain observed at hyperpolarized potentials is a result of increased functional coupling between LCCs (L-type Ca(2+) channels) and RyRs (ryanodine-sensitive Ca(2+) release channels). We also demonstrate mechanisms by which alterations in the early repolarization phase of the action potential, resulting from reduction of the transient outward potassium current, alters properties of EC coupling."
1 . Greenstein JL, Hinch R, Winslow RL (2006) Mechanisms of excitation-contraction coupling in an integrative model of the cardiac ventricular myocyte. Biophys J 90(1):77-91 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Neuron or other electrically excitable cell;
Brain Region(s)/Organism:
Cell Type(s): Heart cell; Cardiac ventricular cell;
Channel(s): I L high threshold; I Potassium; I Calcium;
Gap Junctions:
Simulation Environment: MATLAB;
Model Concept(s): Action Potentials;
Search NeuronDB for information about:  I L high threshold; I Calcium; I Potassium;
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