We have described in rat basilar arterial myocytes, that in the absence of extracellular Ca2+ influx, activation of L-type Ca2+ channels is coupled to Ca2+ release from the sarcoplasmic reticulum (del Valle-Rodriguez et al, 2003). This mechanism, denoted as calcium channel-induced Ca2+ release (CCICR), depends on the conformational change of L-type Ca2+ channels and the downstream activation of the G protein-phospholipase C (PLC) biochemical cascade, leading to synthesis of InsP3 and vasoconstriction in the absence of extracellular calcium. We have investigated whether CCICR is present in coronary arterial myocytes. We measured cytosolic Ca2+ concentration in isolated myocytes by microfluorimetry and arterial tension was monitored by using a Mulvany-Halpern myograph. In isolated myocytes 70K+ solution induced calcium release in the absence of extracellular calcium.Ca2+ channel activation induced by depolarization or by FPL-64176 (FPL), a Ca2+ channel agonist, evoked arterial ring constriction in the absence of extracellular calcium that was suppressed by Ca2+ channels antagonists as nifedipine, diltiazem or D-600. Using a pharmacological approach we tested whether the metabotropic cascade activated by Ca2+ channel activation is involved in the vasoconstriction induced by FPL. Exposure of arterial rings to U73122, a PLC inhibitor, significantly reduced the force induced by the Ca2+ channel agonist. The role of sarcoplasmic reticulum was studied using inhibitors of InsP3 and Ryanodine receptors such as 2-APB and tetracaine respectively. Both agents significantly inhibited the vasoconstriction induced by FPL. These results suggest that in the coronary artery, contraction can be triggered by Ca2+ channel activation in the absence of external Ca2+ through a metabotropic Ca2+-channel activation and Ca2+ release from internal stores.