Аннотация
Computer simulation was used to investigate the calcium levels after
sarcolemmal calcium influx through L-type calcium channels (DHPRs)
into the narrow diadic space of cardiac muscle. The effect of various
cytosolic and membranebound buffers, diad geometry, DHPR properties
(open time and current), and surface charge were examined. The simulations
showed that phospholipid binding sites on the sarcolemmal membrane
are the major buffer affecting free calcium (Ca$^2+$) levels
in the diad. The inclusion of surface charge effects calculated from
Gouy-Chapman theory resulted in a marked decrease in Ca$^2+$
levels at all times and a faster decay of Ca$^2+$ after termination
of DHPR influx. For a DHPR current of 200 fA, Ca$^2+$ at the
center of the diad reached peak levels of approximately 73 microM.
In larger diads (> or = 400 nm diameter), Ca$^2+$ decayed more
slowly than in smaller diads (100-200 nm diameter), although peak
Ca$^2+$ levels reached during typical DHPR open times were
similar. For a wide range of DHPR single-channel current magnitudes
(Ica = 25-200 fA), Ca$^2+$ levels in the diad were approximately
proportional to ICa. The decrease in calculated Ca$^2+$ levels
due to the effects of surface charge can be interpreted as resulting
from an effective "volume expansion" of the diad space. Furthermore,
the layer of increased Ca$^2+$ close to the sarcolemmal membrane
can act as a fast buffer.
- 9199775
- binding
- calcium
- calcium,
- cardiovascular,
- cell
- channel
- channel,
- channels,
- computer
- cytosol,
- factors,
- gating,
- gov't,
- heart,
- ion
- kinetics,
- l-type,
- mathematics,
- membrane,
- models,
- muscle
- myocardium,
- non-u.s.
- proteins,
- receptor
- release
- research
- reticulum,
- ryanodine
- sarcolemma,
- sarcoplasmic
- signal
- simulation,
- sites,
- structural,
- support,
- time
- transduction,
- transport,
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