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MODEL0848116681 - Hund2004_VentricularEpicardialAction

 

The following model is part of the non-curated branch of BioModels Database. While the syntax of the model has been verified, its semantics remains unchecked. Any annotation present in the models is not a product of BioModels' annotators. We are doing our best to incorporate this model into the curated branch as soon as possible. In the meantime, we display only limited metadata here. For further information about the model, please download the SBML file.


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Reference Publication
Publication ID: 15505083
Hund TJ, Rudy Y.
Rate dependence and regulation of action potential and calcium transient in a canine cardiac ventricular cell model.
Circulation 2004 Nov; 110(20): 3168-3174
Department of Biomedical Engineering, Washington University, St. Louis, MO 63130-4899, USA.  [more]
Model
Original Model: CellML logo
Submitter: Vijayalakshmi Chelliah
Submission Date: 29 Apr 2009 14:58:40 UTC
Last Modification Date: 29 Apr 2009 14:58:40 UTC
Creation Date: 29 Apr 2009 14:58:40 UTC
Encoders:
bqbiol:occursIn Brenda Tissue Ontology cardiac muscle fiber
bqbiol:hasTaxon Taxonomy Canis lupus familiaris
bqbiol:isVersionOf Gene Ontology cardiac muscle cell action potential
Notes

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

This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
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To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.

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