Rate dependence and regulation of action potential and calcium transient in a canine cardiac ventricular cell model.

ABSTRACT:

Background

Computational biology is a powerful tool for elucidating arrhythmogenic mechanisms at the cellular level, where complex interactions between ionic processes determine behavior. A novel theoretical model of the canine ventricular epicardial action potential and calcium cycling was developed and used to investigate ionic mechanisms underlying Ca2+ transient (CaT) and action potential duration (APD) rate dependence.

Methods and results

The Ca2+/calmodulin-dependent protein kinase (CaMKII) regulatory pathway was integrated into the model, which included a novel Ca2+-release formulation, Ca2+ subspace, dynamic chloride handling, and formulations for major ion currents based on canine ventricular data. Decreasing pacing cycle length from 8000 to 300 ms shortened APD pri

SUBMITTER: Hund TJ 

PROVIDER: S-EPMC1851913 | biostudies-literature | 2004 Nov

REPOSITORIES: biostudies-literature