Hypoxia and cyanide induce depolarization and catecholamine release in dispersed guinea‐pig chromaffin cells
Hypoxia and cyanide induce depolarization and catecholamine release in dispersed guinea‐pig chromaffin cells
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缺氧和氰化物诱导分散的豚鼠嗜铬细胞去极化和儿茶酚胺释放
DOI：
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发表时间：
1998
期刊：
影响因子：
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通讯作者：
I. Imanaga
中科院分区：
文献类型：
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作者：
Masumi Inoue;N. Fujishiro;I. Imanaga
[1]采用穿孔膜片法和电流分析法测定肾上腺髓质细胞本身是否具有缺氧感受能力，以及缺氧感受如何被转换为儿茶酚胺（CA）分泌。2缺氧、氰化物（CN）或毒蕈碱促进了分离的嗜铬细胞CA的分泌。CN诱导的分泌不受去除葡萄糖的影响，表明CN释放是由于化学缺氧。3.去Ca ~（2+）或应用Cd ~（2+）或甲氧维拉帕米（D-600）均能明显抑制CN和毒蕈碱诱导的分泌。4氰化物和毒蕈碱产生去极化，产生动作电位，并增加细胞内Ca 2+浓度，使用乙酰氧基甲基（AM）酯形式的fluo-3在存在外部Ca 2+离子的情况下测定，但不存在外部Ca 2+离子。5缺氧和CN在Cl−离子的平衡电位下产生内向电流，无论细胞中是否存在Na+离子，用N-甲基-D-葡萄糖胺替代灌注液中的134 mM Na+离子，CN电流抑制71%。在标准灌注液中，CN电流的逆转电位为−24 mV。6缺氧、CN和毒蕈碱诱导的电流与超极化平行降低，CN可阻止毒蕈碱（而非尼古丁）诱导进一步的内向电流。7我们得出结论，缺氧和CN通过去极化和随后的电压依赖性Ca 2+通道的激活诱导CA分泌，并且这种去极化是由于阳离子通道的开放，其可能与毒蕈碱阳离子通道相同。
1 The perforated patch method and amperometry were used to determine whether the adrenal medullary cell itself is capable of sensing hypoxia and, if so, how such sensation is transduced to secretion of catecholamines (CA). 2 Exposure to hypoxia, cyanide (CN), or muscarine facilitated CA secretion from dissociated chromaffin cells. The CN‐induced secretion was not affected by removal of glucose, indicating that the CN release is due to chemical hypoxia. 3 The secretions induced by CN and muscarine were markedly diminished by removal of Ca2+ ions or by application of Cd2+ or methoxyverapamil (D‐600). 4 Cyanide and muscarine produced depolarizations with generation of action potentials and increased intracellular Ca2+ concentrations determined using the acetoxymethyl (AM) ester form of fluo‐3 in the presence of external Ca2+ ions, but not in their absence. 5 Hypoxia and CN produced inward currents at an equilibrium potential for Cl− ions, irrespective of whether or not Na+ ions were present in the cells, and substitution of N‐methyl‐D‐glucamine for 134 mM Na+ ions in the perfusate inhibited the CN current by 71 %. The reversal potential for the CN current was −24 mV in the standard perfusate. 6 The hypoxia‐, CN‐ and muscarine‐induced currents decreased in parallel with hyperpolarizations, and exposure to CN prevented muscarine, but not nicotine, from inducing a further inward current. 7 We conclude that hypoxia and CN induce CA secretion through depolarization and the subsequent activation of voltage‐dependent Ca2+ channels and that this depolarization is due to opening of cation channels, which are possibly identical to muscarinic cation channels.
DOI：
10.1172/jci115326
发表时间：
1991-08
期刊：
The Journal of clinical investigation
影响因子：
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作者：
B. A. Molitoris;A. Geerdes;J R McIntosh
通讯作者：
B. A. Molitoris;A. Geerdes;J R McIntosh