Changes in Intracellular Ca2+ Induced with Adrenaline in Swine Lingual Artery

Background and Objectives: Dental doctors routinely infiltrate adrenaline combined with lidocaine into the oral mucosa. However, they do not well know the physiological characteristics and mechanisms of contraction induced by adrenaline in the oral maxillofacial artery. We investigated the changes in the intracellular Ca2+ concentration by an adrenaline-induced contraction in the swine lingual artery. Materials and Methods: We prepared artery rings with denuded endothelium and simultaneously measured tension and intracellular Ca2+ concentration ([Ca2+]i). The effects of adrenaline in the presence or absence of intracellular Ca2+ on artery rings and verapamil on Ca2+ influx activated by adrenaline were assessed. Results: In the presence of intracellular Ca2+, the application of adrenaline caused a rapid increase in tension and [Ca2+ i, which then decreased slowly. In the absence of extracellular Ca2+, adrenaline caused a transient increase in [Ca2+]i and tension. The application of adrenaline in the presence of extracellular Ca2+ after depletion of the intracellular Ca2+ store caused a slow increase in [Ca2+]i and tension, while co-treatment with verapamil inhibited the increases in [Ca2+]intracellular and tension was induced by adrenaline. The tension relationship obtained with adrenaline was located on the left of the [Ca2+]i-tension relation curve obtained with KCl. Conclusions: The induction of contraction may involve three mechanisms: (1) Release of Ca2+ from the intracellular store, (2) influx of extracellular Ca2+ through voltage-gated Ca2+ channels, and (3) the Ca2+ sensitivity of the contractile apparatus.