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首页> 外文期刊>Cellular Signalling >Morphine and anandamide stimulate intracellular calcium transients in human arterial endothelial cells: coupling to nitric oxide release.
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Morphine and anandamide stimulate intracellular calcium transients in human arterial endothelial cells: coupling to nitric oxide release.

机译:吗啡和anandamide刺激人动脉内皮细胞中的细胞内钙瞬变:与一氧化氮的释放耦合。

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Both morphine and anandamide significantly stimulated cultured endothelial intracellular calcium level increases in a concentration-dependent manner in cells pre-loaded with fura 2/AM. Morphine is more potent than anandamide (approximately 275 vs. 135 nM [Ca]i), and the [Ca]i for both ligands was blocked by prior exposure of the cells to their respective receptor antagonist, i.e., naloxone and SR 171416A. Various opioid peptides did not exhibit this ability, indicating a morphine-mu3-mediated process. In comparing the sequence of events concerning morphine's and anandamide's action in stimulating both [Ca]i and nitric oxide production in endothelial cells, we found that the first event precedes the second by 40+/-8 sec. The opiate and cannabinoid stimulation of [Ca]i was attenuated in cells leeched of calcium, strongly suggesting that intracellular calcium levels regulate cNOS activity.
机译:吗啡和anandamide均显着刺激了预先装有呋喃2 / AM的细胞中培养的内皮细胞内钙水平以浓度依赖的方式增加。吗啡比anandamide更有效(约275 vs. 135 nM [Ca] i),两种配体的[Ca] i都可以通过事先将细胞暴露于其各自的受体拮抗剂即纳洛酮和SR 171416A来阻断。各种阿片样肽均未表现出这种能力,表明吗啡-mu3介导的过程。在比较有关吗啡和阿南酰胺在刺激内皮细胞中Ca 1和一氧化氮产生中的作用的事件顺序时,我们发现第一个事件比第二个事件先发生40 +/- 8秒。钙的阿片类药物和大麻素对钙的刺激作用减弱,这强烈表明细胞内钙水平调节cNOS活性。

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