Ohara-Imaizumi M, Miyakawa Y, Kumakura K
Life Science Institute, Sophia University, Tokyo, Japan.
Neurosci Lett. 1988 Nov 11;93(2-3):294-9. doi: 10.1016/0304-3940(88)90098-5.
Characteristics of the inhibitory action of clonidine on catecholamine release in bovine adrenal chromaffin cells were investigated. Clonidine at 3 x 10(-5) M inhibited acetylcholine (ACh)-evoked release by about 50%, but not catecholamine release evoked by high K+. Another alpha 2-agonist alpha-methyladrenaline was ineffective at inhibiting ACh-evoked release. The inhibition by clonidine of ACh-evoked release was not reversed by alpha 2-antagonists. Treatment of these cells with pertussis toxin reversed the inhibitory effect of clonidine, while it did not affect the inhibitory action of hexamethonium and of nifedipine. Therefore, clonidine inhibition of catecholamine release in these cells seems not to be mediated by the alpha 2-adrenoceptor, but might be mediated by a specific receptor for clonidine.
研究了可乐定对牛肾上腺嗜铬细胞儿茶酚胺释放的抑制作用特性。3×10⁻⁵ M的可乐定抑制乙酰胆碱(ACh)诱发的释放约50%,但不抑制高钾诱发的儿茶酚胺释放。另一种α₂ - 激动剂α - 甲基肾上腺素对抑制ACh诱发的释放无效。可乐定对ACh诱发释放的抑制作用不能被α₂ - 拮抗剂逆转。用百日咳毒素处理这些细胞可逆转可乐定的抑制作用,而它不影响六甲铵和硝苯地平的抑制作用。因此,可乐定对这些细胞儿茶酚胺释放的抑制作用似乎不是由α₂ - 肾上腺素能受体介导的,而是可能由可乐定的特异性受体介导。