Yamada Y, Teraoka H, Nakazato Y, Ohga A
Department of Pharmacology, Faculty of Veterinary Medicine, Hokkaido University, Sapporo, Japan.
Neurosci Lett. 1988 Aug 1;90(3):338-42. doi: 10.1016/0304-3940(88)90212-1.
Unlike acetylcholine, caffeine was much more effective in releasing catecholamine in the absence of extracellular Ca2+ than in its presence in perfused cat adrenal glands. The intracellular Ca2+ antagonist, TMB-8 (10(-4) M), inhibited reversibly the catecholamine secretion evoked by caffeine (40 mM) and that induced by acetylcholine (10(-4) M) in the presence of hexamethonium (10(-3) M) during perfusion with Ca2+-free Locke solution containing EGTA (10(-5) M). These results support our view that muscarinic receptor activation causes catecholamine secretion by mobilizing Ca2+ from an intracellular pool just as caffeine does.
与乙酰胆碱不同,在灌注的猫肾上腺中,咖啡因在无细胞外Ca2+时比有细胞外Ca2+时更有效地释放儿茶酚胺。细胞内Ca2+拮抗剂TMB-8(10^(-4)M)在含有EGTA(10^(-5)M)的无钙洛克溶液灌注期间,可逆地抑制了咖啡因(40mM)诱发的儿茶酚胺分泌以及六甲铵(10^(-3)M)存在时乙酰胆碱(10^(-4)M)诱导的儿茶酚胺分泌。这些结果支持了我们的观点,即毒蕈碱受体激活通过像咖啡因那样从细胞内储存库动员Ca2+来引起儿茶酚胺分泌。