Background: Although lidocaine is a commonly used local anesthetic in dental treatment, the effects of lidocaine on calcium release in craniofacial arteries such as the lingual artery are not well known. Aims: The aim of this study was to examine the effects of lidocaine on calcium release and the role of pathways in swine lingual artery contraction induced with agonists. Materials and Methods: We measured intracellular Ca2+ concentration ([Ca2+]i) and tension using front-surface fluorometry in sections of swine lingual artery with denuded endothelium. Results: The [Ca2+]i and tension induced with adrenaline and histamine in the absence of extracellular Ca2+ with lidocaine added were low compared with or without lidocaine, while the [Ca2+]i and tension induced with caffeine were the same with or without lidocaine. Treatment with lidocaine before and during the application of adrenaline significantly inhibited the increase in [Ca2+]i and tension induced with adrenaline in the presence of extracellular Ca2+ after depletion of the intracellular Ca2+ store. Conclusions: Lidocaine depressed increases in [Ca2+]i and tension that were dependent on the Ca2+ via inositol trisphosphate channel-operated Ca2±entry channels, and lidocaine did not attenuate Ca2±induced Ca2+ release in KCl- and agonist-induced smooth muscle contraction. Lidocaine depressed the increase of Ca2+ influx from extracellular Ca2+ through RACC or nonselective cation channels. Schlagwörter: lidocaine, caffeine, intracellular Ca2+ concentration, inositol trisphosphate channel, L-type channel