Yokoyama K, Yagasaki O
Department of Veterinary Pharmacology, College of Agriculture, University of Osaka Prefecture, Japan.
Jpn J Pharmacol. 1990 Jan;52(1):109-14. doi: 10.1254/jjp.52.109.
In the present study, we investigated the effects of various Ca2+ blockers on the release of acetylcholine (ACh) induced by nicotine, electrical field stimulation (EFS) and high-K+. Cd2+ markedly depressed the ACh release due to these stimuli. Verapamil inhibited the nicotine-induced ACh release remarkably and the EFS- or the high-K(+)-induced ACh release to a lesser extent. Since the nicotine- and the EFS-induced ACh releases were inhibited by procaine, the local anesthetic property of verapamil likely contributes in part to the inhibition. Diltiazem abolished the nicotine-induced ACh release completely but did not affect the EFS-induced release and significantly increased the high-K(+)-induced ACh release. These results suggest the absolute requirement for extracellular Ca2+ in the release of ACh induced by nicotine as well as EFS and high-K+. In addition, these stimuli may open the same Ca2+ channel to evoke ACh release.
在本研究中,我们研究了各种钙离子阻滞剂对尼古丁、电场刺激(EFS)和高钾诱导的乙酰胆碱(ACh)释放的影响。镉离子(Cd2+)显著抑制了由这些刺激引起的ACh释放。维拉帕米显著抑制尼古丁诱导的ACh释放,对EFS或高钾诱导的ACh释放的抑制作用较小。由于普鲁卡因抑制了尼古丁和EFS诱导的ACh释放,维拉帕米的局部麻醉特性可能部分促成了这种抑制作用。地尔硫卓完全消除了尼古丁诱导的ACh释放,但不影响EFS诱导的释放,且显著增加了高钾诱导的ACh释放。这些结果表明,尼古丁、EFS和高钾诱导的ACh释放绝对需要细胞外钙离子。此外,这些刺激可能打开相同的钙离子通道以引发ACh释放。