<?xml version='1.0' encoding='utf-8'?>
<!-- FILE : schuster_model_2003.xml
CREATED : 20th January 2004
LAST MODIFIED : 20th January 2004
AUTHOR : Catherine Lloyd
Bioengineering Instute
The University of Auckland
MODEL STATUS : This model conforms to the CellML 1.0 Specification released on
10th August 2001, and the 16/01/2002 CellML Metadata 1.0 Specification.
DESCRIPTION : This file contains a CellML description of Schuster et al.'s 2003 mathematical model of the electrophysiological endothelial cell response to bradykinin.
CHANGES:
-->
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<title>Modelling the Electrophysiological Endothelial Cell Response to Bradykinin</title>
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<firstname>Catherine</firstname>
<surname>Lloyd</surname>
<affiliation>
<shortaffil>Auckland Bioengineering Institute, The University of Auckland</shortaffil>
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<title>Model Status</title>
<para>
This CellML model runs in OpenCell and COR but does not relicate the published results. There are unit inconsistencies which need fixing. Also in the absence of published initial conditions/parameter values for Cai, IP3 and C, arbitary values were used. Further, there is no defining equation or paramter value for PoSKCa (the probability of the SK_Ca channel being open).
</para>
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<sect1 id="sec_structure">
<title>Model Structure</title>
<para>
ABSTRACT: The goal of the present study is to construct a biophysical model of the coronary artery endothelial cell response to bradykinin. This model takes into account intracellular Ca2+ dynamics, membrane potential, a non-selective cation channel, and two Ca(2+)-dependent K+ channels, as well as intra- and extracellular Ca2+ sources. The model reproduces the experimental data available, and predicts certain quantities which would be hard to obtain experimentally, like the individual K+ channel currents when the membrane potential is allowed to freely evolve, the implication of epoxyeicosatrienoic acids (EETs), and the total K+ released during stimulation. The main results are: (1) the large-conductance K+ channel participates only very little in the overall response; (2) EETs are required in order to explain the experimental current-potential relationships, but are not an essential component of the bradykinin response; and (3) the total K+ released during stimulation gives rise to a concentration in the intercellular space which is of millimolar order. This concentration change is compatible with the hypothesis that K+ contributes to the endothelium-derived hyperpolarizing factor phenomenon.
</para>
<para>
The original paper reference is cited below:
</para>
<para>
Modelling the electrophysiological endothelial cell response to bradykinin, Alexander Schuster, Jean-Louis Beny, and Jean-Jacques Meister, 2003, <emphasis>European Biophysics Journal</emphasis>, 32, 370-380. <ulink url="http://www.ncbi.nlm.nih.gov/pubmed/12851795">PubMed ID: 12851795</ulink>
</para>
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<caption>Schematic diagram of the model, describing the electrophysiological endothelial cell response to bradykinin.</caption>
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Modelling the electrophysiological endothelial cell response to bradykinin
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The University of Auckland, Auckland Bioengineering Institute
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<vCard:Given>Catherine</vCard:Given>
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Schuster et al.'s 2003 mathematical model of the electrophysiological endothelial cell response to bradykinin.
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