Hilgemann1987_CalciumTransients

This a model from the article:
Excitation-contraction coupling and extracellular calcium transients in rabbit
atrium: reconstruction of basic cellular mechanisms.

Hilgemann DW, Noble D. Proc R Soc Lond B Biol Sci
1987 Mar 23;230(1259):163-205 2884668
,
Abstract:

Interactions of electrogenic sodium-calcium exchange, calcium channel and
sarcoplasmic reticulum in the mammalian heart have been explored by simulation
of extracellular calcium transients measured with tetramethylmurexide in rabbit
atrium. The approach has been to use the simplest possible formulations of these
mechanisms, which together with a minimum number of additional mechanisms allow
reconstruction of action potentials, intracellular calcium transients and
extracellular calcium transients. A 3:1 sodium-calcium exchange stoichiometry is
assumed. Calcium-channel inactivation is assumed to take place by a
voltage-dependent mechanism, which is accelerated by a rise in intracellular
calcium; intracellular calcium release becomes a major physiological regulator
of calcium influx via calcium channels. A calcium release mechanism is assumed,
which is both calcium- and voltage-sensitive, and which undergoes prolonged
inactivation. 200 microM cytosolic calcium buffer is assumed. For most
simulations only instantaneous potassium conductances are simulated so as to
study the other mechanisms independently of time- and calcium-dependent outward
current. Thus, the model reconstructs extracellular calcium transients and
typical action-potential configuration changes during steady-state and
non-steady-state stimulation from the mechanisms directly involved in
trans-sarcolemmal calcium movements. The model predicts relatively small
trans-sarcolemmal calcium movements during regular stimulation (ca. 2 mumol kg-1
fresh mass per excitation); calcium current is fully activated within 2 ms of
excitation, inactivation is substantially complete within 30 ms, and
sodium-calcium exchange significantly resists repolarization from approximately
-30 mV. Net calcium movements many times larger are possible during
non-steady-state stimulation. Long action potentials at premature excitations or
after inhibition of calcium release can be supported almost exclusively by
calcium current (net calcium influx 5-30 mumol kg-1 fresh mass); action
potentials during potentiated post-stimulatory contractions can be supported
almost exclusively by sodium-calcium exchange (net calcium efflux 4-20 mumol
kg-1 fresh mass). Large calcium movements between the extracellular space and
the sarcoplasmic reticulum can take place through the cytosol with virtually no
contractile activation. The simulations provide integrated explanations of
electrical activity, contractile function and trans-sarcolemmal calcium
movements, which were outside the explanatory range of previous models.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Hilgemann DW, Noble D. (1987) - version06

The original CellML model was created by:
Noble, Penny, J

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