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紫外线诱导离体大鼠主动脉光舒张的机制

Mechanism of UV light-induced photorelaxation in isolated rat aorta.

作者信息

Kim J H, Hong Y, Shim C S

机构信息

College of Veterinary Medicine and Institute of Animal Medicine, Gyeongsang National University, Jinju 660-701, Korea.

出版信息

J Vet Sci. 2000 Dec;1(2):81-6.

Abstract

Isolated rat thoracic aorta which is pharmacologically precontracted by phenylephrine induces photorelaxation when exposed to long wave length UV-light. The aim of the present study was to characterize the mechanism of UV-light induced by photorelaxation in the rat aorta. 1. UV light relaxed both endothelium-intact and -denuded rat aortic rings contracted by phenylephrine. The magnitude of relaxation on UV light was dependent on the exposure time and slightly greatly in endothelium-denuded rings than in endothelium-intact preparations. 2. L-NAME (10 nM-100 uM) but not D-NAME completely inhibited the photorelaxation in a concentration dependent manner. 3. The UV-induced relaxation was inhibited by methylene blue (1 -100 uM), and verapamil (100 nM), and removal of extracellular Ca2+. In contrast, UV-light induced photorelaxation was potentiated by N(w)-nitro-Larginine (L-NOARG) treatment. 4. In immunocytochemical analysis of UV-light induced iNOS and eNOS expression in rat aortas, at which expression levels were increased in a time-dependent manner on UV-irradiation in aortic endothelium and smooth muscle, respectively. These results suggest that UV light-induced photorelaxation may be due to nitric oxide from exogenously administered L-arginine as well as endogenous nitric oxide donors such as amino acid and arginine derivatives. Additional suggestion is that UV light stimulates the expression of nitric oxide synthases, and its activity for nitric oxide generation is dependent on cytosolic Ca2+ originated from extracellular space.

摘要

用去甲肾上腺素进行药理学预收缩的离体大鼠胸主动脉,在暴露于长波长紫外光时会诱导光舒张。本研究的目的是阐明大鼠主动脉中紫外光诱导光舒张的机制。1. 紫外光可使去甲肾上腺素收缩的完整内皮和去内皮大鼠主动脉环舒张。紫外光诱导的舒张幅度取决于照射时间,且去内皮环中的舒张幅度略大于完整内皮制剂。2. L-NAME(10 nM - 100 μM)而非D-NAME以浓度依赖性方式完全抑制光舒张。3. 亚甲蓝(1 - 100 μM)、维拉帕米(100 nM)以及去除细胞外Ca2+可抑制紫外诱导的舒张。相反,N(ω)-硝基-L-精氨酸(L-NOARG)处理可增强紫外光诱导的光舒张。4. 在对紫外光诱导大鼠主动脉中诱导型一氧化氮合酶(iNOS)和内皮型一氧化氮合酶(eNOS)表达的免疫细胞化学分析中,主动脉内皮和平滑肌中iNOS和eNOS的表达水平在紫外照射后均呈时间依赖性增加。这些结果表明,紫外光诱导的光舒张可能归因于外源性给予的L-精氨酸产生的一氧化氮以及内源性一氧化氮供体,如氨基酸和精氨酸衍生物。另一个推测是,紫外光刺激一氧化氮合酶的表达,其产生一氧化氮的活性依赖于源自细胞外空间的胞质Ca2+。

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