Serotonin uptake by bovine pulmonary artery endothelial cells in culture. II. Stimulation by hypoxia.

Serotonin uptake by bovine pulmonary artery endothelial cells in culture. II. Stimulation by hypoxia.
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培养物中牛肺动脉内皮细胞对血清素的摄取。

DOI:
10.1152/ajpcell.1986.250.5.c766
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发表时间:
1986
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Fanburg,BL
Fanburg,BL
中科院分区:
--
文献类型:
--
作者:
Lee,SL;Fanburg,BL

文献摘要

被引文献

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暴露于3%O2的牛肺动脉内皮细胞在24-48小时后,5-羟色胺(5-HT)摄取的刺激约为2倍时,细胞暴露于20%O2。当细胞再次置于20%O2中48 h后,增强的摄取被逆转。在暴露于缺氧0.5或2 h后未观察到刺激。当异丙肼阻断5-HT向5-羟基吲哚-3-乙酸的转化时,存在刺激,这表明通过增强单胺氧化酶活性没有发生增强的摄取。缺氧刺激摄取发生在低浓度的5-HT(高达10(-6)M),但不发生在高浓度的5-HT(大于10(-5)M),并被丙咪嗪或缺乏钠从培养基中阻断,表明高亲和力的运输,而不是扩散的5-HT刺激。此外,细胞暴露于缺氧并没有产生损伤或蛋白质含量变化或台盼蓝排斥的形态学证据。3%O2暴露48 h后细胞数与对照组相比略有减少。3%O_2对细胞ATP含量无明显影响,对细胞培养液中乳酸脱氢酶含量无明显影响。因此,暴露于培养的内皮细胞缺氧刺激5-HT积累的膜活性,没有证据表明对细胞的损伤。
Exposure of bovine pulmonary artery endothelial cells to 3% O2 resulted in approximately twofold stimulation of serotonin (5-HT) uptake after 24-48 h when compared with cells exposed to 20% O2. The enhanced uptake was reversed after 48 h when cells were again placed in 20% O2. The stimulation was not observed after 0.5 or 2 h of exposure to hypoxia. The stimulation was present when iproniazid blocked conversion of 5-HT to 5-hydroxyindole-3-acetic acid, indicating that enhanced uptake did not occur through augmentation of monoamine oxidase activity. Stimulation of uptake by hypoxia occurred at low concentrations of 5-HT (up to 10(-6) M) but not at high 5-HT concentrations (greater than 10(-5) M) and was blocked by imipramine or absence of sodium from the medium, indicating that high-affinity transport and not diffusion of 5-HT was stimulated. Furthermore, exposure of cells to hypoxia did not produce morphological evidence of injury or change in protein content or trypan blue exclusion. The cell number of 3% O2-exposed cells was slightly reduced when compared with controls after 48 h. There was no change in cellular ATP or increase in lactate dehydrogenase in medium of cells exposed to 3% O2. Thus exposure of endothelial cells in culture to hypoxia stimulates the membrane activity of 5-HT accumulation with no evidence of injury to the cell.