Sarai2003_CardiacSAnodePacemaker

This a model from the article:
Role of individual ionic current systems in the SA node hypothesized by a model
study.

Sarai N, Matsuoka S, Kuratomi S, Ono K, Noma A. Jpn J Physiol
2003 Apr;53(2):125-34 12877768
,
Abstract:

This paper discusses the development of a cardiac sinoatrial (SA) node pacemaker
model. The model successfully reconstructs the experimental action potentials at
various concentrations of external Ca2+ and K+. Increasing the amplitude of
L-type Ca2+ current (I(CaL)) prolongs the duration of the action potential and
thereby slightly decreases the spontaneous rate. On the other hand, a negative
voltage shift of I(CaL) gating by a few mV markedly increases the spontaneous
rate. When the amplitude of sustained inward current (I(st)) is increased, the
spontaneous rate is increased irrespective of the I(CaL) amplitude. Increasing
[Ca2+](o) shortens the action potential and increases the spontaneous rate. When
the spontaneous activity is stopped by decreasing I(CaL) amplitude, the resting
potential is nearly constant (-35 mV) over 1-15 mM [K+](o) as observed in the
experiment. This is because the conductance of the inward background
non-selective cation current balances with the outward [K+](o)-dependent K+
conductance. The unique role of individual voltage- and time-dependent ion
channels is clearly demonstrated and distinguished from that of the background
current by calculating an instantaneous zero current potential ("lead
potential") during the course of the spontaneous activity.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Sarai N, Matsuoka S, Kuratomi S, Ono K, Noma A. (2003) - version=1.0

The original CellML model was created by:
Alan Garny

[e-mail]
The University of Oxford
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