Dataset Information

Courtemanche1998_AtrialActionPotential

ABSTRACT: This a model from the article: Ionic mechanisms underlying human atrial action potential properties: insights from a mathematical model. Courtemanche M, Ramirez RJ, Nattel S. Am J Physiol 1998 Jul;275(1 Pt 2):H301-21 9688927 , Abstract: The mechanisms underlying many important properties of the human atrial action potential (AP) are poorly understood. Using specific formulations of the K+, Na+, and Ca2+ currents based on data recorded from human atrial myocytes, along with representations of pump, exchange, and background currents, we developed a mathematical model of the AP. The model AP resembles APs recorded from human atrial samples and responds to rate changes, L-type Ca2+ current blockade, Na+/Ca2+ exchanger inhibition, and variations in transient outward current amplitude in a fashion similar to experimental recordings. Rate-dependent adaptation of AP duration, an important determinant of susceptibility to atrial fibrillation, was attributable to incomplete L-type Ca2+ current recovery from inactivation and incomplete delayed rectifier current deactivation at rapid rates. Experimental observations of variable AP morphology could be accounted for by changes in transient outward current density, as suggested experimentally. We conclude that this mathematical model of the human atrial AP reproduces a variety of observed AP behaviors and provides insights into the mechanisms of clinically important AP properties. This model was taken from the CellML repository and automatically converted to SBML. The original model was: Courtemanche M, Ramirez RJ, Nattel S. (1998) - version03 The original CellML model was created by: Noble, Penny, J penny.noble@dpag.ox.ac.uk Oxford University Department of Physiology, Anatomy & Genetics 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.

SUBMITTER: Vijayalakshmi Chelliah

PROVIDER: MODEL0913049417 | BioModels | 2005-01-01

REPOSITORIES: BioModels

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	MODEL0913049417?filename=MODEL0913049417-biopax2.owl	Owl
	MODEL0913049417?filename=MODEL0913049417-biopax3.owl	Owl
	MODEL0913049417?filename=MODEL0913049417.m	Other
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Ionic mechanisms underlying human atrial action potential properties: insights from a mathematical model.

Courtemanche M M Ramirez R J RJ Nattel S S

The American journal of physiology 19980701 1

The mechanisms underlying many important properties of the human atrial action potential (AP) are poorly understood. Using specific formulations of the K+, Na+, and Ca2+ currents based on data recorded from human atrial myocytes, along with representations of pump, exchange, and background currents, we developed a mathematical model of the AP. The model AP resembles APs recorded from human atrial samples and responds to rate changes, L-type Ca2+ current blockade, Na+/Ca2+ exchanger inhibition, a ...[more]

PMID: 9688927

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