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MODEL0847712949 - Kurata2002_SinoatrialNode


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: 12384487
Kurata Y, Hisatome I, Imanishi S, Shibamoto T.
Dynamical description of sinoatrial node pacemaking: improved mathematical model for primary pacemaker cell.
Am. J. Physiol. Heart Circ. Physiol. 2002 Nov; 283(5): H2074-101
Department of Physiology, Kanazawa Medical University, 1-1 Daigaku, Uchinada-machi, Kahoku-gun, Ishikawa 920-0293, Japan.  [more]
Original Model: CellML logo
Submitter: Vijayalakshmi Chelliah
Submission Date: 29 Apr 2009 11:25:55 UTC
Last Modification Date: 29 Apr 2009 11:25:55 UTC
Creation Date: 29 Apr 2009 11:25:55 UTC
bqmodel:isDerivedFrom PubMed 8166247
PubMed 1722117
PubMed 10899081
PubMed 8869126
bqbiol:occursIn Brenda Tissue Ontology sinus node
bqbiol:hasTaxon Taxonomy Oryctolagus cuniculus
bqbiol:isVersionOf Gene Ontology SA node cell action potential

This a model from the article:
Dynamical description of sinoatrial node pacemaking: improved mathematical model for primary pacemaker cell.
Kurata Y, Hisatome I, Imanishi S, Shibamoto T. Am J Physiol Heart Circ Physiol 2002 Nov;283(5):H2074-101 12384487 ,
We developed an improved mathematical model for a single primary pacemaker cell of the rabbit sinoatrial node. Original features of our model include 1) incorporation of the sustained inward current (I(st)) recently identified in primary pacemaker cells, 2) reformulation of voltage- and Ca(2+)-dependent inactivation of the L-type Ca(2+) channel current (I(Ca,L)), 3) new expressions for activation kinetics of the rapidly activating delayed rectifier K(+) channel current (I(Kr)), and 4) incorporation of the subsarcolemmal space as a diffusion barrier for Ca(2+). We compared the simulated dynamics of our model with those of previous models, as well as with experimental data, and examined whether the models could accurately simulate the effects of modulating sarcolemmal ionic currents or intracellular Ca(2+) dynamics on pacemaker activity. Our model represents significant improvements over the previous models, because it can 1) simulate whole cell voltage-clamp data for I(Ca,L), I(Kr), and I(st); 2) reproduce the waveshapes of spontaneous action potentials and ionic currents during action potential clamp recordings; and 3) mimic the effects of channel blockers or Ca(2+) buffers on pacemaker activity more accurately than the previous models.

This model was taken from the CellML repository and automatically converted to SBML.
The original model was: Kurata Y, Hisatome I, Imanishi S, Shibamoto T. (2002) - version05
The original CellML model was created by:
Noble, Penny,
The University of Oxford

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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.