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Ethanol inhibits L-arginine uptake and enhances NO formation in human placenta

机译:乙醇抑制L-精氨酸的摄取并增加人胎盘中NO的形成

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The acute effects of ethanol (20 - 60 mM) on L-arginine uptake and nitric oxide (NO) formation was investigated in human placental cotyledons perfused at constant flow. Ethanol (40 mM) decreased L-[H-3]arginine uptake from 27.6 +/- 2.3 to 15.8 +/- 1.3 per cent (P< 0.05) of the injected dose and significantly enhanced NO levels in the perfusate from 0.88 lus/minus> 0.11 to 2.80 +/- 0.39 muM. Ethanol also elicited the constriction of placental vessels. The effects of ethanol (20 - 60 mM) on L-arginine uptake and endothelial NO synthase (eNOS) activity were also investigated in cultured human umbilical vein endothelial cells (HUVEC). After 60 min of ethanol (40 mM) exposure, basal L-[H-3]arginine uptake (4.7 +/- 03 pmol/mug protein/min) was inhibited by 60 per cent (P< 0.05). Basal eNOS activity in HUVEC determined under "no flow" (static) conditions was significantly increased ( 1.8 fold) by 60 mM ethanol. These data are consistent with a stimulatory effect of ethanol on eNOS activity in both basal and flow-stimulated conditions, which may serve a protective role against its vasoconstrictive acute effect. While acute ethanol administration inhibits L-arginine uptake, the present results do not allow us to speculate on the effects of chronic ethanol exposure on NO formation in the fetoplacental unity. (C) 2001 Elsevier Science Inc. All rights reserved. [References: 39]
机译:在以恒定流量灌注的人胎盘子叶中,研究了乙醇(20-60 mM)对L-精氨酸摄取和一氧化氮(NO)形成的急性影响。乙醇(40 mM)将L- [H-3]精氨酸的摄取量从注射剂量的27.6 +/- 2.3降低至15.8 +/- 1.3%(P <0.05),灌注液中的NO水平从0.88 lus /负> 0.11至2.80 +/-0.39μM。乙醇还会引起胎盘血管的收缩。还研究了培养的人脐静脉内皮细胞(HUVEC)中乙醇(20-60 mM)对L-精氨酸摄取和内皮一氧化氮合酶(eNOS)活性的影响。在乙醇(40 mM)暴露60分钟后,基础L- [H-3]精氨酸摄取(4.7 +/- 03 pmol /杯蛋白/分钟)被抑制60%(P <0.05)。通过60 mM乙醇,在“无流量”(静态)条件下测定的HUVEC中的基础eNOS活性显着提高(<相似> 1.8倍)。这些数据与乙醇对基础和血流刺激条件下eNOS活性的刺激作用相一致,这可能对其血管收缩性急性作用起保护作用。虽然急性乙醇给药会抑制L-精氨酸的摄取,但目前的结果使我们无法推测慢性乙醇暴露对胎儿胎盘素中NO形成的影响。 (C)2001 Elsevier Science Inc.保留所有权利。 [参考:39]

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