Calcium-dependent contractile activation of cerebral artery produced by quick stretch

Quick stretch of helical strips of rabbit basilar artery at a rate of 4-50 cm/s to 140% of the initial muscle length evoked phasic contraction. The contraction was potentiated by cardiac glycosides, tetraethylammonium, and high K+, all of which augment transmembrane influx of Ca2+, and the enhanced response was suppressed by Ca2+-antagonists such as verapamil and nifedipine. The stretch-induced contraction in Ca2+-free medium was progressively reduced depending on the number of stretches during the observation period of 90 min. The response to quick stretch in Ca2+-free solution was enhanced by norepinephrine or histamine but was not affected by high K+ (40-100 mM), verapamil, or nifedipine. These results suggest that contraction of rabbit basilar artery produced by quick stretch depends not only on transmembrane supply of Ca2+ but also on release of Ca2% bound to the membrane or in internal depots. It also seems possible that, in addition to depolarization of the membrane, mechanical deformation itself triggers the release of Ca2+.