ABSTRACT:
This a model from the article:
Rate dependence and regulation of action potential and calcium transient in a
canine cardiac ventricular cell model.
Hund TJ, Rudy Y. Circulation
2004 Nov 16;110(20):3168-74 15505083
,
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 primarily because of I(Ca(L)) reduction, with additional
contributions from I(to1), I(NaK), and late I(Na). CaT amplitude increased as
cycle length decreased from 8000 to 500 ms. This positive rate-dependent
property depended on CaMKII activity. CONCLUSIONS: CaMKII is an important
determinant of the rate dependence of CaT but not of APD, which depends on
ion-channel kinetics. The model of CaMKII regulation may serve as a paradigm for
modeling effects of other regulatory pathways on cell function.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Hund TJ, Rudy Y. (2004) - version03
The original CellML model was created by:
Noble, Penny
penny.noble@dpag.ox.ac.uk
University of Oxford
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Vijayalakshmi Chelliah 