Hund2004_VentricularEpicardialAction

  public model
Short description

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.

Format
SBML (L2V3)
Related Publication
  • Rate dependence and regulation of action potential and calcium transient in a canine cardiac ventricular cell model.
  • Hund TJ, Rudy Y
  • Circulation , 11/ 2004 , Volume 110 , pages: 3168-3174
  • Department of Biomedical Engineering, Washington University, St. Louis, MO 63130-4899, USA.
  • 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.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.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.
Contributors
Vijayalakshmi Chelliah

Metadata information

is
BioModels Database MODEL0848116681
isDescribedBy
PubMed 15505083
hasTaxon
isVersionOf
hasProperty
Mathematical Modelling Ontology Ordinary differential equation model
occursIn
Brenda Tissue Ontology cardiac muscle fiber
Curation status
Non-curated
Original model(s)
http://www.cellml.org/models/hund_rudy_2004_version03
  • Model originally submitted by : Vijayalakshmi Chelliah
  • Submitted: 29-Apr-2009 14:58:40
  • Last Modified: 29-Apr-2009 14:58:40
Revisions
  • Version: 2 public model Download this version
    • Submitted on: 29-Apr-2009 14:58:40
    • Submitted by: Vijayalakshmi Chelliah
    • With comment: Current version of Hund2004_VentricularEpicardialAction
  • Version: 1 public model Download this version
    • Submitted on: 29-Apr-2009 14:58:40
    • Submitted by: Vijayalakshmi Chelliah
    • With comment: Original import of Hund2004_VentricularEpicardialAction