(1999) We present a model of the canine midmyocardial ventricular action potential and Ca2+ transient. The model is used to estimate the degree of functional upregulation and downregulation of Na/Ca exchanger protein and sarcoplasmic reticulum Ca ATPase in heart failure using data obtained from 2 different experimental protocols. (2000): A model of canine I:(to1) (the Ca(2+)-independent transient outward current) is formulated as the combination of Kv4.3 and Kv1.4 currents and is incorporated into an existing canine ventricular myocyte model. Simulations demonstrate strong coupling between L-type Ca(2+) current and I:(Kv4.3) and predict a bimodal relationship between I:(Kv4.3) density and APD whereby perturbations in I:(Kv4.3) density may produce either prolongation or shortening of APD, depending on baseline I:(to1) current level. See each paper for more and details.
Model Type: Neuron or other electrically excitable cell
Currents: I L high threshold; I A; I K; I Calcium; I Potassium
Model Concept(s): Ion Channel Kinetics; Heart disease
Simulation Environment: Java
Implementer(s): Bassingthwaighte, James; Li, Zheng
References:
Greenstein JL, Wu R, Po S, Tomaselli GF, Winslow RL. (2000). Role of the calcium-independent transient outward current I(to1) in shaping action potential morphology and duration. Circulation research 87 [PubMed]
Winslow RL, Rice J, Jafri S, Marbán E, O'Rourke B. (1999). Mechanisms of altered excitation-contraction coupling in canine tachycardia-induced heart failure, II: model studies. Circulation research 84 [PubMed]