ブタ舌動脈血管平滑筋におけるアドレナリン収縮に対するリドカインの抑制機序の検討

抄録

The purpose of this study was to clarify the effects and mechanisms of lidocaine (1.0×10^-3M)on changes in contraction of the smooth muscle induced by voltage dependent Ca²⁺ channel (VDCC) stimulator, KCl(90mM), and receptor activated Ca²⁺ channel (RACC) agonist, adrenaline(2×10^-5M), in porcine lingual arteries.
The isometric tension and intracellular Ca²⁺ concentration ( [Ca²⁺]i) by the fura-2 microfluorometric methods were measured simultaneously, and from them we tried to deduce the depressing mechanism of lidocaine (1.0×10^-3M) on the contraction.
The results were obtained as follows:
(1) Lidocaine depressed the increase of contraction and [Ca²⁺]i induced by KCl and adrenaline in a concentration-dependent manner.
(2) Lidocaine depressed the increase of contraction and [Ca²⁺]i induced by adrenaline in normal physiological salt solution after depletion of the intracellular Ca²⁺-sensitive Ca²⁺ store.
(3) Lidocaine depressed the increase of contraction and [Ca²⁺]i induced by adrenaline in Ca²⁺-free physiological salt solution.
(4) Lidocaine had no effect on Ca²⁺ induced Ca²⁺ release(CICR) by caffein. These results suggest the following conclusions as follows,
1. Lidocaine depresses influx of Ca^{2+ t}hrough VDCC and RACC. 2. Lidocaine inhibits the increase of [Ca²⁺]i through IP₃ processes. 3. Lidocaine has no effect on CICR.