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学科主题基础医学
Hypoxia-induced reactive oxygen species downregulate ETB receptor-mediated contraction of rat pulmonary arteries
Wang, XH; Tong, M; Chinta, S; Raj, JU; Gao, YS
关键词superoxide endothelin
刊名AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
2006-03-01
DOI10.1152/ajplung.00262.2005
290期:3页:L570-L578
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Physiology ; Respiratory System
研究领域[WOS]Physiology ; Respiratory System
关键词[WOS]NITRIC-OXIDE ; SUPEROXIDE-DISMUTASE ; NEWBORN LAMBS ; IN-VIVO ; VASOCONSTRICTION ; ENDOTHELIN-1 ; EXPRESSION ; CELLS ; ET-1 ; HYPERTENSION
英文摘要

Production of reactive oxygen species (ROS) may be increased during hypoxia in pulmonary arteries. In this study, the role of ROS in the effect of hypoxia on endothelin ( ET) type B (ETB) receptor- mediated vasocontraction in lungs was determined. In rat intrapulmonary (similar to 0.63 mm ID) arteries, contraction induced by IRL-1620 (a selective ETB receptor agonist) was significantly attenuated after 4 h of hypoxia (30 mmHg Po-2) compared with normoxic control (140 mmHg Po-2). The effect was abolished by tiron, a scavenger of superoxide anions, but not by polyethylene glycol ( PEG)- conjugated catalase, which scavenges H2O2. The hypoxic effect on ETB receptor- mediated vasoconstriction was also abolished by endothelium denudation but not by nitro-L-arginine and indomethacin. Exposure for 4 h to exogenous superoxide anions, but not H2O2, attenuated the vasoconstriction induced by IRL-1620. Confocal study showed that hypoxia increased ROS production in pulmonary arteries that were scavenged by PEG-conjugated SOD. In endothelium-intact pulmonary arteries, the ETB receptor protein was reduced after 4 h of exposure to hypoxia, exogenous superoxide anions, or ET-1. BQ-788, a selective ETB receptor antagonist, prevented these effects. ET-1 production was stimulated in endothelium-intact arteries after 4 h of exposure to hypoxia or exogenous superoxide anions. This effect was blunted by PEG-conjugated SOD. These results demonstrate that exposure to hypoxia attenuates ETB receptor- mediated contraction of rat pulmonary arteries. A hypoxia-induced production of superoxide anions may increase ET-1 release from the endothelium and result in downregulation of ETB receptors on smooth muscle.

语种英语
WOS记录号WOS:000235182700019
引用统计
被引频次:26[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/66308
专题基础医学院_心血管所
作者单位1.Biomed Res Inst, Los Angeles, CA USA
2.Peking Univ, Dept Physiol & Pathophysiol, Hlth Sci Ctr, Beijing 100083, Peoples R China
3.Peking Univ, Key Lab Mol Cardiovasc Sci, Minist Educ, Beijing 100083, Peoples R China
4.Univ Calif Los Angeles, Div Neonatol, Harbor UCLA Med Ctr, Geffen Sch Med, Los Angeles, CA USA
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Wang, XH,Tong, M,Chinta, S,et al. Hypoxia-induced reactive oxygen species downregulate ETB receptor-mediated contraction of rat pulmonary arteries[J]. AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY,2006,290(3):L570-L578.
APA Wang, XH,Tong, M,Chinta, S,Raj, JU,&Gao, YS.(2006).Hypoxia-induced reactive oxygen species downregulate ETB receptor-mediated contraction of rat pulmonary arteries.AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY,290(3),L570-L578.
MLA Wang, XH,et al."Hypoxia-induced reactive oxygen species downregulate ETB receptor-mediated contraction of rat pulmonary arteries".AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY 290.3(2006):L570-L578.
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