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 Ca
2+ channel (VDCC) stimulator, KCl(90mM), and receptor activated Ca
2+ channel (RACC) agonist, adrenaline(2×10
-5M), in porcine lingual arteries.
The isometric tension and intracellular Ca
2+ concentration ( [Ca
2+]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 [Ca
2+]i induced by KCl and adrenaline in a concentration-dependent manner.
(2) Lidocaine depressed the increase of contraction and [Ca
2+]i induced by adrenaline in normal physiological salt solution after depletion of the intracellular Ca
2+-sensitive Ca
2+ store.
(3) Lidocaine depressed the increase of contraction and [Ca
2+]i induced by adrenaline in Ca
2+-free physiological salt solution.
(4) Lidocaine had no effect on Ca
2+ induced Ca
2+ release(CICR) by caffein. These results suggest the following conclusions as follows,
1. Lidocaine depresses influx of Ca
2+ through VDCC and RACC. 2. Lidocaine inhibits the increase of [Ca
2+]i through IP
3 processes. 3. Lidocaine has no effect on CICR.
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