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紫外线照射的人内皮细胞会产生一氧化氮,一氧化氮可能会引发血管舒张反应。

Ultraviolet-irradiated human endothelial cells elaborate nitric oxide that may evoke vasodilatory response.

作者信息

Deliconstantinos G, Villiotou V, Fassitsas C

机构信息

Department of Experimental Physiology, University of Athens Medical School, Greece.

出版信息

J Cardiovasc Pharmacol. 1992;20 Suppl 12:S63-5. doi: 10.1097/00005344-199204002-00019.

DOI:10.1097/00005344-199204002-00019
PMID:1282989
Abstract

Human skin absorbs solar ultraviolet radiation which evokes vasodilation by a mechanism that is unknown. In this work, we show that ultraviolet (290-320 nm) irradiation of cultured human endothelial cells with doses (60 mJ/cm2) evoked nitric oxide (NO) release that was sustained for more than 60 min. In addition to augmenting NO, cyclic GMP production by human endothelial cells was also increased in a time-dependent manner. Ultraviolet stimulation of NO production was also observed with the enzyme NO synthase purified from the cytosol of human endothelial cells. These results indicate that ultraviolet radiation stimulates NO release, which stimulates cyclic GMP production by vascular smooth muscle, which results in a relaxation response.

摘要

人体皮肤会吸收太阳紫外线辐射,其通过一种未知机制引起血管舒张。在这项研究中,我们发现,用剂量为60 mJ/cm2的紫外线(290 - 320 nm)照射培养的人内皮细胞,会引发一氧化氮(NO)释放,且这种释放可持续超过60分钟。除了增加NO外,人内皮细胞中环鸟苷酸(cGMP)的生成也呈时间依赖性增加。从人内皮细胞胞质溶胶中纯化得到的一氧化氮合酶,在紫外线刺激下也会产生NO。这些结果表明,紫外线辐射刺激NO释放,进而刺激血管平滑肌产生cGMP,最终导致舒张反应。

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