Hallam T J, Pearson J D
FEBS Lett. 1986 Oct 20;207(1):95-9. doi: 10.1016/0014-5793(86)80019-9.
Cultured piglet endothelial cells were grown to confluence on glass coverslips and loaded with the fluorescent Ca2+ indicator, fura-2. Using a dual-wavelength excitation fluorescence spectrophotometer it was found that ATP caused a rapid transient elevation in [Ca2+]i in the presence of extracellular calcium which decreased to a maintained elevated level. With no extracellular calcium ATP evoked a similar transient increase which returned to the basal level. Addition of 50 mM K+ had no effect on [Ca2+]i or on the effect of ATP on [Ca2+]i in the presence of extracellular Ca2+. The data suggest that ATP causes both discharge of calcium from an intracellular pool and influx across the plasma membrane although this is unlikely to be via a voltage-operated channel. ATP stimulated simultaneously the production of PGI2 to a similar extent in the presence or absence of extracellular calcium. Elevated [Ca2+]i may be an important activation pathway in the endothelial cell.
将培养的仔猪内皮细胞在玻璃盖玻片上培养至汇合,并加载荧光钙指示剂fura-2。使用双波长激发荧光分光光度计发现,在细胞外钙存在的情况下,ATP导致细胞内钙离子浓度([Ca2+]i)迅速短暂升高,随后降至维持的升高水平。在无细胞外钙的情况下,ATP引起类似的短暂升高,然后恢复到基础水平。添加50 mM K+对细胞外钙存在时的[Ca2+]i或ATP对[Ca2+]i的作用没有影响。数据表明,ATP导致钙离子从细胞内储存库释放以及跨质膜内流,尽管这不太可能通过电压门控通道。无论细胞外钙是否存在,ATP均能同时刺激前列环素(PGI2)产生至相似程度。细胞内钙离子浓度升高可能是内皮细胞中的重要激活途径。