镁离子和咖啡因诱导人血管内皮细胞内钙离子释放
Mg2+ and caffeine-induced intracellular Ca2+ release in human vascular endothelial cells.
作者信息
Zhang A, Cheng T P, Altura B T, Altura B M
机构信息
Department of Physiology, State University of New York, Brooklyn 11203.
出版信息
Br J Pharmacol. 1993 Jun;109(2):291-2. doi: 10.1111/j.1476-5381.1993.tb13568.x.
Interaction of ionized magnesium ([Mg2+]o) and caffeine in regulation of intracellular free calcium concentration ([Ca2+]i) in human aortic endothelial cells was studied using fura-2 and digital imaging microscopy. In 1.2 mM [Mg2+]o, basal [Ca2+]i was 73.7 +/- 22.4 nM, with a heterogeneous distribution within the cells. No significant changes of basal [Ca2+]i were found either when cells were treated with 10 mM caffeine or when [Mg2+]o was lowered from 1.2 mM to 0.3 mM. However, a combined superfusion of the cells with 0.3 mM [Mg2+]o and 10 mM caffeine resulted in a significant elevation of [Ca2+]i to 382.8 +/- 57.1 nM, probably by release of Ca2+ from internal stores, which was attenuated by NiCl2 (1 mM). These results suggest that a Ca(2+)-induced Ca2+ release mechanism is involved in regulation of [Ca2+]i in endothelial cells, which may be either regulated or modulated by Mg2+.
采用fura - 2和数字成像显微镜研究了离子化镁（[Mg2 + ]o）与咖啡因在调节人主动脉内皮细胞内游离钙浓度（[Ca2 + ]i）中的相互作用。在1.2 mM [Mg2 + ]o条件下，基础[Ca2 + ]i为73.7±22.4 nM，在细胞内呈异质性分布。当细胞用10 mM咖啡因处理或[Mg2 + ]o从1.2 mM降至0.3 mM时，基础[Ca2 + ]i均未发现显著变化。然而，细胞同时用0.3 mM [Mg2 + ]o和10 mM咖啡因进行灌注会导致[Ca2 + ]i显著升高至382.8±57.1 nM，这可能是由于细胞内钙库释放Ca2 + 所致，而这种升高会被1 mM的NiCl2减弱。这些结果表明，Ca(2 + )诱导的Ca2 + 释放机制参与了内皮细胞中[Ca2 + ]i的调节，并且该机制可能受Mg2 + 的调控或调节。
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