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| 氧化应激在D5多巴胺受体基因敲除小鼠血压升高中的作用研究 | |
| 引用本文： | 杨志伟,曾春雨,秦川. 氧化应激在D5多巴胺受体基因敲除小鼠血压升高中的作用研究[J]. 中国比较医学杂志, 2006, 16(3): 129-134,F0002 |
| 作者姓名： | 杨志伟 曾春雨 秦川 |
| 作者单位： | 1. 中国医学科学院实验动物研究所,北京,100080 2. 第三军医大学大坪医院(野战外科研究所)心内科心血管病研究室,重庆,400042 3. Department of Pediatrics, Georgetown University Medical Center, Washington, DC, USA 4. Department of Molecular and Human Genetics and Mitochondrial Diagnostic Laboratory,Baylor College of Medicine, Houston, Texas, USA 5. Department of Pathology, University of Virginia Health Sciences Center, VA, USA |
| 摘 要： | 目的探讨还原型辅酶Ⅱ（NADPH）氧化酶在D5受体基因敲除（D5-/-）小鼠血压升高发生机理中的作用.方法利用第六代D5-/-小鼠和其对照（D5＋/＋）小鼠,检测其肾脏NADPH氧化酶的活性和表达;利用D5受体基因转染的HEK-293细胞作为研究对象,刺激D5受体,研究D5受体对超氧阴离子（O2^-）和过氧化氢（H2O2）的影响.结果 D5-/-小鼠的血压、肾脏NADPH氧化酶的活性和p47^phox蛋白的表达均明显高于D5＋/＋小鼠.多巴胺D5受体激动剂Fenoldopam可降低D5转染HEK-293细胞的O2^-和H2O2的产量.结论氧化应激和NADPH氧化酶活性增强参与了D5-/-小鼠血压升高的发生过程,多巴胺D5受体具有抗氧化应激的功能. |
| 关 键 词： | D5受体 高血压 氧化应激 |
| 文章编号： | 1671-7856（2006）03-0129-06 |
| 收稿时间： | 2006-02-23 |
| 修稿时间： | 2006-02-23 |
The Mechanism of Dopamine D5 Receptor Regulation Hypertension via NADPH Oxidase |
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| YU Pei-ying,WONG Lee-jun,Felder Robin A,Jose Pedro A,YANG Zhi-wei,ZENG Chun-yu,YU Pei-ying,WONG Lee-jun,QIN Chuan,Felder Robin A,Jose Pedro A. The Mechanism of Dopamine D5 Receptor Regulation Hypertension via NADPH Oxidase[J]. Chinese Journal of Comparative Medicine, 2006, 16(3): 129-134,F0002 | |
| Authors: | YU Pei-ying WONG Lee-jun Felder Robin A Jose Pedro A YANG Zhi-wei ZENG Chun-yu YU Pei-ying WONG Lee-jun QIN Chuan Felder Robin A Jose Pedro A |
| Abstract: | Objective To investigate the mechanism(s) of dopamine D_5 receptor regulation to hypertension involved in the antioxidant actions.Methods We investigated blood pressures in D_5 receptor deficient(D_5-/-) and wild type(D_5 / ) mice,and NADPH oxidase protein expression(p47~(phox)) and activity in kidney of those mice.We also checked super oxide and hydrogen peroxide production by using HEK-293 cells heterologously expressing human D_5 receptor.Result The systolic,diastolic and mean arterial blood pressures,and NADPH oxidase activity and p47~(phox) expression were higher in D_5-/-than D_5 / mice.In HEK-293 cells heterologously expressing human D_5 receptor,its agonist,fenoldopam,decreased super oxide and hydrogen peroxide production.Conclusion The ability of D_5 receptor stimulation to inhibit NADPH oxidase activity so as to decrease ROS production may explain,in part,the antihypertensive action of D_5 receptor activation. |
| Keywords: | Dopamine D5 receptor Hypertension Reactive oxygen species |
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