Mitochondrial inhibitors evoke catecholamine release from pheochromocytoma cells.
Mitochondrial inhibitors evoke catecholamine release from pheochromocytoma cells.
复制标题
线粒体抑制剂引起嗜铬细胞瘤细胞释放儿茶酚胺。
DOI：
10.1006/bbrc.2000.2894
复制
发表时间：
2000
影响因子：
3.1
通讯作者：
C. Peers
中科院分区：
文献类型：
--
作者：
S. Taylor;S. M. Shaw;C. Peers
采用电流分析法，以真实的时间监测暴露于线粒体抑制剂和解偶联剂引起的单个嗜铬细胞瘤（PC 12）细胞的量子儿茶酚胺分泌。氰化物（0.05-5 mM）引起电流事件频率的浓度依赖性增加。通过去除细胞外Ca（2+）和应用电压门控Ca（2+）通道的非选择性阻断剂Cd（2+）（200 μ M），这种分泌反应被消除。钙也能抑制分泌。用ω-芋螺毒素GVIA预处理细胞以选择性抑制N型Ca（2+）通道后，75%。当细胞暴露于鱼藤酮（10 μ M），二硝基苯酚（250 μ M）和p-三氟甲氧基苯腙（1 μ M）时，也检测到分泌，至于氰化物，这些分泌反应被消除细胞外Ca（2+）或应用200 μ M Cd（2+）。这些结果表明，与缺氧一样，线粒体抑制剂和解偶联剂引起PC 12细胞分泌儿茶酚胺，这完全依赖于通过电压门控Ca（2+）通道的Ca（2+）内流。
Quantal catecholamine secretion evoked from individual pheochromocytoma (PC12) cells by exposure to mitochondrial inhibitors and uncouplers was monitored in real time using amperometry. Cyanide (0.05-5 mM) caused a concentration-dependent increase in the frequency of amperometric events. This secretory response was abolished by removal of extracellular Ca(2+) and by the application of Cd(2+) (200 microM), a nonselective blocker of voltage-gated Ca(2+) channels. Secretion was also inhibited by ca. 75% following pretreatment of cells with omega-conotoxin GVIA to inhibit N-type Ca(2+) channels selectively. Secretion was also detected when cells were exposed to rotenone (10 microM), dinitrophenol (250 microM) and p-trifluoromethoxyphenyl hydrazone (1 microM) and, as for cyanide, these secretory responses were abolished by removal of extracellular Ca(2+) or application of 200 microM Cd(2+). These results indicate that, like hypoxia, mitochondrial inhibitors and uncouplers evoke catecholamine secretion from PC12 cells which is wholly dependent on Ca(2+) influx through voltage-gated Ca(2+) channels.