We have described in rat basilar artery that L type Ca2+ channel activation can activate Ca2+ release from sarcoplasmic reticulum (SR) in the absence of extracellular Ca2+ through a metabotropic pathway (mechanism denoted as Calcium-Channel Induced Calcium Release, CCICR) (Del Valle-Rodriguez et al., 2003). The calcium-release mechanism depends on the conformational change of L-type Ca2+ channels and the downstream activation of the G protein/phospholipase C (PLC) cascade, leading to synthesis of InsP3 and Ca2+ release from the SR. Because previous results were obtained in isolated myocytes bathed in free Ca2+ medium, the aim of this work was to study the functional role of CCICR in physiological conditions (i.e. in arteries bathed in medium containing Ca2+). Experiments were done in rat cerebral arteries obtained from anaesthetized (sodium pentobarbital, 50 mg/Kg, ip.) animals of weight 250-300 g (30 rats and 100 arterial rings). Isometric force and cytosolic Ca2+ concentration ([Ca2+]i) were measured in rat basilar arterial rings and in intact arteries. Ca2+ channel activation produced an initial rapid rise in cytosolic Ca2+ and a second plateau phase that was maintained until the end of the stimulus. Concomitant with this change in [Ca2+]i, a reduction of the arterial diameter was detected. Both signals were transient when Ca2+ was eliminated from the extracellular medium. Cyclopiazonic acid, ryanodine and U73122, inhibitors of SR Ca2+ pump, ryanodine receptors and PLC respectively, reduced the maintained phase of contraction whereas the transient component was not significantly affected. Our results suggest that in physiological conditions Ca2+ channel-induced contraction of the basilar artery can be mediated by both Ca2+ influx from the extracellular medium (ionotropic function of Ca2+ channel) and Ca2+ release from the SR through a metabotropic pathway.