(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.
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. Circ Res 87:1026-33 [PubMed]
Winslow RL, Rice J, Jafri S, Marban E, O'Rourke B (1999) Mechanisms of altered excitation-contraction coupling in canine tachycardia-induced heart failure, II: model studies. Circ Res 84:571-86 [PubMed]