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Department of Physiological Sciences, Lund University, S-223 62 Lund, Sweden
To investigate
the Ca2+-dependent plasticity of
sarcoplasmic reticulum (SR) function in vascular smooth muscle,
transient responses to agents releasing intracellular
Ca2+ by either ryanodine
(caffeine) or
D-myo-inositol
1,4,5-trisphosphate [IP3;
produced in response to norepinephrine (NE),
5-hydroxytryptamine (5-HT), arginine vasopressin (AVP)] receptors
in rat tail arterial rings were evaluated after 4 days of organ
culture. Force transients induced by all agents were increased compared
with those induced in fresh rings. Stimulation by 10% FCS
during culture further potentiated the force and
Ca2+ responses to caffeine (20 mM)
but not to NE (10 µM), 5-HT (10 µM), or AVP (0.1 µM). The effect
was persistent, and SR capacity was not altered after reversible
depletion of stores with cyclopiazonic acid. The effects of serum could
be mimicked by culture in depolarizing medium (30 mM
K+) and blocked by the addition
of verapamil (1 µM) or EGTA (1 mM) to the medium, lowering
intracellular Ca2+ concentration
([Ca2+]i)
during culture. These results show that modulation of SR function can
occur in vitro by a mechanism dependent on long-term levels of basal
[Ca2+]i
and involving ryanodine- but not
IP3 receptor-mediated
Ca2+
release.
sarcoplasmic reticulum; organ culture; tail artery; D-myo-inositol 1,4,5-trisphosphate
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