• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

一氧化氮在动脉粥样硬化进展和消退中的作用。

Role of nitric oxide in progression and regression of atherosclerosis.

作者信息

Cooke J P

机构信息

Division of Cardiovascular Medicine, Stanford University School of Medicine, CA 94305-5246, USA.

出版信息

West J Med. 1996 May;164(5):419-24.

PMID:8686299
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1303540/
Abstract

Endothelium-derived nitric oxide is a potent endogenous vasodilator that is derived from the metabolism of L-arginine. This endothelial factor inhibits circulating blood elements from interacting with the vessel wall. Platelet adherence and aggregation as well as monocyte adherence and infiltration are opposed by this paracrine substance. By virtue of these characteristics, endothelium-derived nitric oxide inhibits atherogenesis in animal models and may even induce regression.

摘要

内皮源性一氧化氮是一种强效的内源性血管舒张剂,由L-精氨酸代谢产生。这种内皮因子可抑制循环血液成分与血管壁相互作用。这种旁分泌物质可对抗血小板黏附和聚集以及单核细胞黏附和浸润。凭借这些特性,内皮源性一氧化氮在动物模型中可抑制动脉粥样硬化的发生,甚至可能促使其消退。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee6b/1303540/2362427d877c/westjmed00356-0036-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee6b/1303540/2362427d877c/westjmed00356-0036-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee6b/1303540/2362427d877c/westjmed00356-0036-a.jpg

相似文献

1
Role of nitric oxide in progression and regression of atherosclerosis.一氧化氮在动脉粥样硬化进展和消退中的作用。
West J Med. 1996 May;164(5):419-24.
2
[Endothelial factors and thrombocyte function].
Z Kardiol. 1991;80 Suppl 5:3-6.
3
[Nitric oxide: the endogenous nitrate in the cardiovascular system].[一氧化氮:心血管系统中的内源性硝酸盐]
Herz. 1996 Jun;21 Suppl 1:50-60.
4
[Pathogenetic aspects of the L-arginine-NO metabolic pathway in arteriosclerosis and possible therapeutic aspects].
Vasa. 1996;25(4):305-16.
5
Oral L-arginine inhibits platelet aggregation but does not enhance endothelium-dependent dilation in healthy young men.口服L-精氨酸可抑制健康年轻男性的血小板聚集,但不会增强内皮依赖性舒张功能。
J Am Coll Cardiol. 1995 Oct;26(4):1054-61. doi: 10.1016/0735-1097(95)00257-9.
6
Nitric oxide and the proliferation of vascular smooth muscle cells.一氧化氮与血管平滑肌细胞的增殖
Cardiovasc Res. 1999 Aug 15;43(3):580-94. doi: 10.1016/s0008-6363(99)00171-6.
7
Primary endothelial dysfunction: atherosclerosis.原发性内皮功能障碍:动脉粥样硬化。
J Mol Cell Cardiol. 1999 Jan;31(1):23-37. doi: 10.1006/jmcc.1998.0841.
8
The endothelium in acute coronary syndromes.急性冠状动脉综合征中的内皮功能
Eur Heart J. 1998 Apr;19 Suppl C:C30-8.
9
Endothelium-derived factors and peripheral vascular disease.
Cardiovasc Clin. 1992;22(3):3-17.
10
Interactions between endothelial mediators.内皮介质之间的相互作用。
Pharmacol Toxicol. 1995 Jul;77(1):1-9. doi: 10.1111/j.1600-0773.1995.tb01906.x.

引用本文的文献

1
Combined effects of cigarette smoking, alcohol drinking and eNOS Glu298Asp polymorphism on blood pressure in Chinese male hypertensive subjects.吸烟、饮酒和内皮型一氧化氮合酶Glu298Asp基因多态性对中国男性高血压患者血压的联合影响。
Tob Induc Dis. 2019 Aug 2;17:59. doi: 10.18332/tid/110678. eCollection 2019.
2
Effect of Enhanced External Counterpulsation and Cardiac Rehabilitation on Quality of Life, Plasma Nitric Oxide, Endothelin 1 and High Sensitive CRP in Patients With Coronary Artery Disease: A Pilot Study.增强型体外反搏与心脏康复对冠心病患者生活质量、血浆一氧化氮、内皮素-1及高敏C反应蛋白的影响:一项初步研究
Ann Rehabil Med. 2015 Apr;39(2):191-8. doi: 10.5535/arm.2015.39.2.191. Epub 2015 Apr 24.
3

本文引用的文献

1
Regression or progression. Dependency on vascular nitric oxide.消退或进展。对血管一氧化氮的依赖性。
Arterioscler Thromb Vasc Biol. 1996 Jan;16(1):44-50. doi: 10.1161/01.atv.16.1.44.
2
L-arginine inhibits balloon catheter-induced intimal hyperplasia.L-精氨酸可抑制球囊导管诱导的内膜增生。
Biochem Biophys Res Commun. 1993 May 28;193(1):291-6. doi: 10.1006/bbrc.1993.1622.
3
Ischemia-reperfusion in feline small intestine: a role for nitric oxide.猫小肠缺血再灌注:一氧化氮的作用
Association of endothelial nitric oxide synthase polymorphisms with coronary artery disease in Korean individuals with or without diabetes mellitus.
韩国糖尿病患者和非糖尿病患者中内皮型一氧化氮合酶基因多态性与冠状动脉疾病的关联
Exp Ther Med. 2010 Jul;1(4):719-724. doi: 10.3892/etm_00000111. Epub 2010 Jul 1.
4
Ambulatory blood pressure, left ventricular mass and vascular phenotypes in relation to the endothelial nitric oxide synthase gene Glu298Asp and intron 4 polymorphisms in a population-based family study.在一项基于人群的家族研究中,动态血压、左心室质量和血管表型与内皮型一氧化氮合酶基因Glu298Asp及内含子4多态性的关系。
J Hum Hypertens. 2005 May;19(5):413-20. doi: 10.1038/sj.jhh.1001837.
Am J Physiol. 1993 Jan;264(1 Pt 1):G143-9. doi: 10.1152/ajpgi.1993.264.1.G143.
4
Hypercholesterolemia increases endothelial superoxide anion production.高胆固醇血症会增加内皮细胞超氧阴离子的产生。
J Clin Invest. 1993 Jun;91(6):2546-51. doi: 10.1172/JCI116491.
5
Dietary arginine prevents atherogenesis in the coronary artery of the hypercholesterolemic rabbit.饮食中的精氨酸可预防高胆固醇血症兔子冠状动脉的动脉粥样硬化形成。
J Am Coll Cardiol. 1994 Feb;23(2):452-8. doi: 10.1016/0735-1097(94)90433-2.
6
L-arginine improves endothelium-dependent vasorelaxation and reduces intimal hyperplasia after balloon angioplasty.L-精氨酸可改善内皮依赖性血管舒张,并减少球囊血管成形术后的内膜增生。
Arterioscler Thromb. 1994 Jun;14(6):938-43. doi: 10.1161/01.atv.14.6.938.
7
Enhanced endothelial adhesiveness in hypercholesterolemia is attenuated by L-arginine.高胆固醇血症中增强的内皮黏附性被L-精氨酸减弱。
Circulation. 1994 May;89(5):2176-82. doi: 10.1161/01.cir.89.5.2176.
8
Is NO an endogenous antiatherogenic molecule?一氧化氮是一种内源性抗动脉粥样硬化分子吗?
Arterioscler Thromb. 1994 May;14(5):653-5. doi: 10.1161/01.atv.14.5.653.
9
Effect of L-arginine on coronary endothelial function in cardiac transplant recipients. Relation to vessel wall morphology.L-精氨酸对心脏移植受者冠状动脉内皮功能的影响。与血管壁形态的关系。
Circulation. 1994 Apr;89(4):1615-23. doi: 10.1161/01.cir.89.4.1615.
10
Nitric oxide inhibits macrophage-colony stimulating factor gene transcription in vascular endothelial cells.一氧化氮抑制血管内皮细胞中巨噬细胞集落刺激因子基因的转录。
J Biol Chem. 1995 Jul 14;270(28):17050-5. doi: 10.1074/jbc.270.28.17050.