Effects of lidocaine on changes in intracellular Ca²⁺ concentration and tension of the smooth muscle induced by adrenaline in porcine lingual arteries

Abstract

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.