This a model from the article: Mathematical simulations of ligand-gated and cell-type specific effects on the action potential of human atrium. Maleckar MM, Greenstein JL, Trayanova NA, Giles WR. Prog Biophys Mol Biol. 2008; 98(2-3):161-70 19186188 , Abstract: In the mammalian heart, myocytes and fibroblasts can communicate via gap junction, or connexin-mediated current flow. Some of the effects of this electroto nic coupling on the action potential waveform of the human ventricular myocyte have been analyzed in detail. The present study employs a recently developed mathematical model of the human atrial myocyte to investigate the consequences of this heterogeneous cell-cell interaction on the action potential of the human atrium. Two independent physiological processes which alter the physiology of the human atrium have been studied. i) The effects of the autonomic tra nsmitter acetylcholine on the atrial action potential have been investigated by inclusion of a time-independent, acetylcholine-activated K(+) current in th is mathematical model of the atrial myocyte. ii) A non-selective cation current which is activated by natriuretic peptides has been incorporated into a pre viously published mathematical model of the cardiac fibroblast. These results identify subtle effects of acetylcholine, which arise from the nonlinear inte ractions between ionic currents in the human atrial myocyte. They also illustrate marked alterations in the action potential waveform arising from fibrobla st-myocyte source-sink principles when the natriuretic peptide-mediated cation conductance is activated. Additional calculations also illustrate the effect s of simultaneous activation of both of these cell-type specific conductances within the atrial myocardium. This study provides a basis for beginning to as sess the utility of mathematical modeling in understanding detailed cell-cell interactions within the complex paracrine environment of the human atrial myo cardium. This model was taken from the CellML repository and automatically converted to SBML. The original model was: Maleckar MM, Greenstein JL, Trayanova NA, Giles WR. (2009) - version01 The original CellML model was created by: Fink, Martin, martin.fink@dpag.ox.ac.uk The University of Oxford 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.