Yurko K A, Quenzer L F
Life Sci. 1986 Apr 14;38(15):1393-7. doi: 10.1016/0024-3205(86)90472-8.
Trifluoperazine (5-200 microM) stimulated the release of 3H-NE from isolated whole pineal glands in a dose dependent manner. Trifluoperazine-induced release was not dependent on extracellular Ca++, whereas 60 mM K+-evoked release was attenuated in the presence of EGTA and zero Ca++ Krebs. 60 mM K+ and 50 microM trifluoperazine produced an additive effect on 3H-NE release. Clonidine (5 microM) significantly reduced trifluoperazine-induced release by approximately 50% in the presence of Ca++, and in its absence, clonidine significantly attenuated the trifluoperazine response by 42%. Thus trifluoperazine may be acting upon the alpha 2 receptor or intracellular stores of Ca++. These intracellular interactions remain for further study.
三氟拉嗪(5 - 200微摩尔)以剂量依赖的方式刺激离体完整松果体释放3H - 去甲肾上腺素。三氟拉嗪诱导的释放不依赖于细胞外钙离子,而在存在乙二醇双四乙酸(EGTA)和零钙离子的克雷布斯溶液中,60毫摩尔钾离子诱发的释放减弱。60毫摩尔钾离子和50微摩尔三氟拉嗪对3H - 去甲肾上腺素的释放产生相加作用。在有钙离子存在的情况下,可乐定(5微摩尔)使三氟拉嗪诱导的释放显著降低约50%,而在无钙离子的情况下,可乐定使三氟拉嗪反应显著减弱42%。因此,三氟拉嗪可能作用于α2受体或细胞内钙离子储存。这些细胞内相互作用有待进一步研究。