Аннотация
In mammalian cardiac myocytes, calcium released into the dyadic space
rapidly inactivates calcium current (ICa). We used this Ca$^2+$
release-dependent inactivation (RDI) of ICa as a local probe of sarcoplasmic
reticulum Ca$^2+$ release activation. In whole cell patch-clamped
rat ventricular myocytes, Ca$^2+$ entry induced by short prepulses
from -50 mV to positive voltages caused suppression of peak ICa during
a test pulse. The negative correlation between peak ICa suppression
and ICa inactivation during the test pulse indicated that RDI evoked
by the prepulse affected only calcium channels in those dyads in
which calcium release was activated. Ca$^2+$ ions injected during
the prepulse and during the subsequent tail current suppressed peak
ICa in the test pulse to a different extent. Quantitative analysis
indicated that equal Ca$^2+$ charge was 3.5 times less effective
in inducing release when entering during the prepulse than when entering
during the tail. Tail Ca$^2+$ charge injected by the first voltage-dependent
calcium channel (DHPR) openings was three times less effective than
that injected by DHPR reopenings. These findings suggest that calcium
release activation can be profoundly influenced by the recent history
of L-type Ca$^2+$ channel activity due to potentiation of ryanodine
receptors (RyRs) by previous calcium influx. This conclusion was
confirmed at the level of single RyRs in planar lipid bilayers: using
flash photolysis of the calcium cage NP-EGTA to generate two sequential
calcium stimuli, we showed that RyR activation in response to the
second stimulus was four times higher than that in response to the
first stimulus.
- 14522820
- animals,
- calcium
- calcium,
- cardiac,
- cardiovascular,
- channel,
- channels,
- conductivity,
- electric
- gov't,
- male,
- models,
- myocytes,
- non-u.s.
- p.h.s.,
- patch-clamp
- rats,
- receptor
- release
- research
- ryanodine
- stimulation,
- support,
- techniques,
- u.s.
- wistar,
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