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MODEL0847869198 - Jafri1998_VentricularMyocyte

 

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: 9512016
Jafri MS, Rice JJ, Winslow RL.
Cardiac Ca2+ dynamics: the roles of ryanodine receptor adaptation and sarcoplasmic reticulum load.
Biophys. J. 1998 Mar; 74(3): 1149-1168
Department of Biomedical Engineering, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. jafri@bme.jhu.edu  [more]
Model
Original Model: CellML logo
Submitter: Vijayalakshmi Chelliah
Submission Date: 29 Apr 2009 12:35:45 UTC
Last Modification Date: 29 Apr 2009 12:35:45 UTC
Creation Date: 29 Apr 2009 12:35:45 UTC
Encoders:
bqmodel:isDerivedFrom PubMed 8968617
PubMed 7514509
bqbiol:occursIn Brenda Tissue Ontology cardiac muscle fiber
bqbiol:hasTaxon Taxonomy Homo sapiens
bqbiol:isVersionOf Gene Ontology cardiac muscle cell action potential
Notes

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

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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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