Courtemanche1998_AtrialActionPotential

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

[e-mail]
Oxford University
Department of Physiology, Anatomy & Genetics
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