内皮源性活性氧和一氧化氮在去甲肾上腺素诱导的大鼠主动脉环收缩中的作用。
Role of endothelial-derived reactive oxygen species and nitric oxide in norepinephrine-induced rat aortic ring contractions.
作者信息
Srivastava P, Hegde L G, Patnaik G K, Dikshit M
机构信息
Division of Pharmacology, Central Drug Research Institute, Lucknow, PO Box 173, India.
出版信息
Pharmacol Res. 1998 Oct;38(4):265-74. doi: 10.1006/phrs.1998.0357.
In the present investigation involvement of endothelial-derived reactive oxygen species (ROS) and their interaction with nitric oxide (NO), during norepinephrine (NE)-induced contraction of rat aortic rings was studied. NE (1x10(-10) M to 1x10(-5) M) caused concentration-dependent contractio n of the endothelium intact aortic rings. In the presence of hydroxyl radical scavengers, histidine (1x10(-3) M), mannitol (3x10(-3) M), dimethyl sulfoxide (50x10(-3) M) or thiourea (1x10(-3) m), superoxide dismutase (superoxide radical scavenger, SOD 10 or 100 U ml-1) or catalase (hydrogen peroxide inactivator 3, 10, or 100 U ml-1) the concentration-response curve of NE was shifted towards the right. Interestingly, in NG-nitro-l-arginine methyl ester (L-NAME) (1x10(-5) M, a NO synthase inhibitor) pretreated rings, NE-induced contractions were not inhibited by SOD or extracellular hydroxyl radical scavengers (mannitol and histidine). However, in these rings NE-induced contractions were found to be attenuated by endogenous hydroxyl radical scavengers (thiourea and DMSO) or catalase. In the endothelium denuded rings no significant effect of these scavengers on NE-induced contractions was observed. These results thus indicate the involvement of endothelium-derived hydrogen peroxide, superoxide and hydroxyl radicals in the NE-induced contractions. In addition, endothelial NO interacts with the ROS generated during rat aortic ring contractions.
在本研究中，我们探究了内皮源性活性氧（ROS）的参与情况以及它们在去甲肾上腺素（NE）诱导大鼠主动脉环收缩过程中与一氧化氮（NO）的相互作用。NE（1×10⁻¹⁰ M至1×10⁻⁵ M）引起内皮完整的主动脉环浓度依赖性收缩。在存在羟基自由基清除剂（组氨酸，1×10⁻³ M；甘露醇，3×10⁻³ M；二甲基亚砜，50×10⁻³ M或硫脲，1×10⁻³ m）、超氧化物歧化酶（超氧阴离子自由基清除剂，SOD 10或100 U/ml⁻¹）或过氧化氢酶（过氧化氢灭活剂3、10或100 U/ml⁻¹）的情况下，NE的浓度 - 反应曲线向右移动。有趣的是，在经NG - 硝基 - l - 精氨酸甲酯（L - NAME，1×10⁻⁵ M，一种NO合酶抑制剂）预处理的血管环中，NE诱导的收缩不受SOD或细胞外羟基自由基清除剂（甘露醇和组氨酸）的抑制。然而，在这些血管环中，NE诱导的收缩被内源性羟基自由基清除剂（硫脲和二甲基亚砜）或过氧化氢酶减弱。在去内皮的血管环中，未观察到这些清除剂对NE诱导收缩的显著影响。因此，这些结果表明内皮源性过氧化氢、超氧化物和羟基自由基参与了NE诱导的收缩。此外，内皮NO与大鼠主动脉环收缩过程中产生的ROS相互作用。
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