Jafri1998_VentricularMyocyte

  public model
Short description

This a model from the article:
Cardiac Ca2+ dynamics: the roles of ryanodine receptor adaptation and sarcoplasmic reticulum load.
Jafri MS, Rice JJ, Winslow RL. Biophys J 1998 Mar;74(3):1149-68 9512016 ,
Abstract:
We construct a detailed mathematical model for Ca2+ regulation in the ventricular myocyte that includes novel descriptions of subcellular mechanisms based on recent experimental findings: 1) the Keizer-Levine model for the ryanodine receptor (RyR), which displays adaptation at elevated Ca2+; 2) a model for the L-type Ca2+ channel that inactivates by mode switching; and 3) a restricted subspace into which the RyRs and L-type Ca2+ channels empty and interact via Ca2+. We add membrane currents from the Luo-Rudy Phase II ventricular cell model to our description of Ca2+ handling to formulate a new model for ventricular action potentials and Ca2+ regulation. The model can simulate Ca2+ transients during an action potential similar to those seen experimentally. The subspace [Ca2+] rises more rapidly and reaches a higher level (10-30 microM) than the bulk myoplasmic Ca2+ (peak [Ca2+]i approximately 1 microM). Termination of sarcoplasmic reticulum (SR) Ca2+ release is predominately due to emptying of the SR, but is influenced by RyR adaptation. Because force generation is roughly proportional to peak myoplasmic Ca2+, we use [Ca2+]i in the model to explore the effects of pacing rate on force generation. The model reproduces transitions seen in force generation due to changes in pacing that cannot be simulated by previous models. Simulation of such complex phenomena requires an interplay of both RyR adaptation and the degree of SR Ca2+ loading. This model, therefore, shows improved behavior over existing models that lack detailed descriptions of subcellular Ca2+ regulatory mechanisms.

This model was taken from the CellML repository and automatically converted to SBML.
The original model was: Jafri MS, Rice JJ, Winslow RL. (1998) - version03
The original CellML model was created by:
Lloyd, Catherine, May
c.lloyd@aukland.ac.nz
The University of Auckland
The Bioengineering Institute

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.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..

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
  • Cardiac Ca2+ dynamics: the roles of ryanodine receptor adaptation and sarcoplasmic reticulum load.
  • Jafri MS, Rice JJ, Winslow RL
  • Biophysical Journal , 3/ 1998 , Volume 74 , pages: 1149-1168
  • Department of Biomedical Engineering, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. jafri@bme.jhu.edu
  • We construct a detailed mathematical model for Ca2+ regulation in the ventricular myocyte that includes novel descriptions of subcellular mechanisms based on recent experimental findings: 1) the Keizer-Levine model for the ryanodine receptor (RyR), which displays adaptation at elevated Ca2+; 2) a model for the L-type Ca2+ channel that inactivates by mode switching; and 3) a restricted subspace into which the RyRs and L-type Ca2+ channels empty and interact via Ca2+. We add membrane currents from the Luo-Rudy Phase II ventricular cell model to our description of Ca2+ handling to formulate a new model for ventricular action potentials and Ca2+ regulation. The model can simulate Ca2+ transients during an action potential similar to those seen experimentally. The subspace [Ca2+] rises more rapidly and reaches a higher level (10-30 microM) than the bulk myoplasmic Ca2+ (peak [Ca2+]i approximately 1 microM). Termination of sarcoplasmic reticulum (SR) Ca2+ release is predominately due to emptying of the SR, but is influenced by RyR adaptation. Because force generation is roughly proportional to peak myoplasmic Ca2+, we use [Ca2+]i in the model to explore the effects of pacing rate on force generation. The model reproduces transitions seen in force generation due to changes in pacing that cannot be simulated by previous models. Simulation of such complex phenomena requires an interplay of both RyR adaptation and the degree of SR Ca2+ loading. This model, therefore, shows improved behavior over existing models that lack detailed descriptions of subcellular Ca2+ regulatory mechanisms.
Contributors
Vijayalakshmi Chelliah

Metadata information

is
BioModels Database MODEL0847869198
isDescribedBy
PubMed 9512016
hasTaxon
Taxonomy Homo sapiens
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/jafri_rice_winslow_1998_version03
  • Model originally submitted by : Vijayalakshmi Chelliah
  • Submitted: Apr 29, 2009 12:35:45 PM
  • Last Modified: Apr 29, 2009 12:35:45 PM
Revisions
  • Version: 2 public model Download this version
    • Submitted on: Apr 29, 2009 12:35:45 PM
    • Submitted by: Vijayalakshmi Chelliah
    • With comment: Current version of Jafri1998_VentricularMyocyte
  • Version: 1 public model Download this version
    • Submitted on: Apr 29, 2009 12:35:45 PM
    • Submitted by: Vijayalakshmi Chelliah
    • With comment: Original import of Jafri1998_VentricularMyocyte