Аннотация
We have developed a mathematical model of the mouse ventricular myocyte
action potential (AP) from voltage-clamp data of the underlying currents
and Ca$^2+$ transients. Wherever possible, we used Markov models
to represent the molecular structure and function of ion channels.
The model includes detailed intracellular Ca$^2+$ dynamics, with
simulations of localized events such as sarcoplasmic Ca$^2+$
release into a small intracellular volume bounded by the sarcolemma
and sarcoplasmic reticulum. Transporter-mediated Ca$^2+$ fluxes
from the bulk cytosol are closely matched to the experimentally reported
values and predict stimulation rate-dependent changes in Ca$^2+$
transients. Our model reproduces the properties of cardiac myocytes
from two different regions of the heart: the apex and the septum.
The septum has a relatively prolonged AP, which reflects a relatively
small contribution from the rapid transient outward K$^+$ current
in the septum. The attribution of putative molecular bases for several
of the component currents enables our mouse model to be used to simulate
the behavior of genetically modified transgenic mice.
- 15142845
- action
- animals,
- calcium
- calcium,
- cardiac,
- cardiovascular,
- channels,
- chloride
- computer
- conductivity,
- electric
- function,
- gov't,
- homeostasis,
- l-type,
- mice,
- models,
- myocytes,
- non-p.h.s.,
- non-u.s.
- p.h.s.,
- patch-clamp
- potassium
- potentials,
- research
- reticulum,
- sarcoplasmic
- simulation,
- sodium
- support,
- techniques,
- u.s.
- ventricular
- voltage-gated,
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