Stretching releases Ca2+ from intracellular storage sites in canine cerebral arteries

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Abstract
Mechanical stretch applied to canine cerebral artery produced myogenic contraction. The contraction of the artery in response to quick stretch was dependent on not only the transmembrane influx of Ca2+ through 1,4-dihydropyridine-sensitive Ca2+ channels but also the release of Ca2+ from intracellular storage sites: the stretch-produced contractile component that was resistant to 0.1 μM nicardipine, a Ca2+-channel antagonist, was inhibited by about 50% after treatment with ryanodine, and was almost completely suppressed by 0.1 mM 2-nitro-4-carboxyphenyl-N,N-diphenylcarbamate, a putative phospholipase C inhibitor, or by lowering the temperature from 35 to 20 °C. The results suggest that in addition to transmembrane influx of Ca2+ through L-type Ca2+ channels, the release of Ca2+ from both ryanodine-sensitive and -insensitive intracellular storage sites, which increases intracellular Ca2+, accounts for the stretch-induced contraction of canine basilar artery. It seems also possible that inositol 1,4,5-trisphosphate is a common mediator for the release of Ca2+ from both types of intracellular storage sites.Key words: stretch-induced contraction, cerebral artery, phospholipase C, ryanodine, Ca2+ storage sites, inositol 1,4,5-trisphosphate, Ca2+ release, Ca2+-channel antagonist.

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