脑毛细血管内皮细胞中的钠-钾-氯共转运系统：对内皮素和缺氧的反应
Na(+)-K(+)-Cl- cotransport system in brain capillary endothelial cells: response to endothelin and hypoxia.
作者信息
Kawai N, McCarron R M, Spatz M
机构信息
Stroke Branch, National Institute of Neurological Disease and Stroke, National Institutes of Health, Bethesda, Maryland 20892-4128, USA.
出版信息
Neurochem Res. 1996 Oct;21(10):1259-66. doi: 10.1007/BF02532403.
Effect of endothelin-1 and chemically induced hypoxia on Na(+)-K(+)-Cl- cotransport activity in cultured rat brain capillary endothelial cells was examined by using 86Rb+ as a tracer for K+; bumetanide-sensitive K+ uptake was defined as Na(+)-K(+)-Cl- cotransport activity. Endothelin-1, phorbol 12-myristate 13-acetate (PMA), or thapsigargin increased Na(+)-K(+)-Cl- cotransport activity. A protein kinase C inhibitor, bisindolylmaleimide, inhibited PMA- and endothelin-1- (but not thapsigargin-) induced Na(+)-K(+)-Cl- cotransport activity, indicating the presence of both protein kinase C-dependent regulatory mechanisms and protein kinase C-independent mechanisms which involve intracellular Ca2+. Oligomycin, sodium azide, or antimycin A increased Na(+)-K(+)-Cl- cotransport activity by 80-200%. Oligomycin-induced Na(+)-K(+)-Cl- cotransport activity was reduced by an intracellular Ca2+ chelator (BAPTA/AM) but not affected by bisindolylmaleimide, suggesting the involvement of intracellular Ca2+, and not protein kinase C, in hypoxia-induced Na(+)-K(+)-Cl- cotransport activity.
以内皮素 -1 和化学诱导的缺氧对培养的大鼠脑毛细血管内皮细胞中 Na(+)-K(+)-Cl- 共转运活性的影响进行了研究，使用 86Rb+ 作为 K+ 的示踪剂；布美他尼敏感的 K+ 摄取被定义为 Na(+)-K(+)-Cl- 共转运活性。内皮素 -1、佛波酯 12-肉豆蔻酸酯 13-乙酸酯（PMA）或毒胡萝卜素增加了 Na(+)-K(+)-Cl- 共转运活性。一种蛋白激酶 C 抑制剂双吲哚马来酰胺抑制了 PMA 和内皮素 -1（但不包括毒胡萝卜素）诱导的 Na(+)-K(+)-Cl- 共转运活性，表明存在蛋白激酶 C 依赖性调节机制和涉及细胞内 Ca2+ 的蛋白激酶 C 非依赖性机制。寡霉素、叠氮化钠或抗霉素 A 使 Na(+)-K(+)-Cl- 共转运活性增加了 80% - 200%。寡霉素诱导的 Na(+)-K(+)-Cl- 共转运活性被细胞内 Ca2+ 螯合剂（BAPTA/AM）降低，但不受双吲哚马来酰胺影响，这表明在缺氧诱导的 Na(+)-K(+)-Cl- 共转运活性中涉及细胞内 Ca2+ 而非蛋白激酶 C。
Zotero 插件