北京大学医学部机构知识库
Advanced  
IR@PKUHSC  > 北京大学第一临床医学院  > 心血管内科  > 期刊论文
学科主题: 临床医学
题名:
Persistent sodium current and Na+/H+ exchange contributes to the augmentation of the reverse Na+/Ca2+ exchange during hypoxia or acute ischemia in ventricular myocytes
作者: Tang, Qiong1; Ma, Jihua1; Zhang, Peihua1; Wan, Wei1; Kong, Linghao1; Wu, Lin2
关键词: Hypoxia ; Sodium-calcium exchange current ; Persistent sodium current ; Sodium-hydrogen exchange ; Patch-clamp techniques
刊名: PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY
发表日期: 2012-04-01
DOI: 10.1007/s00424-011-1070-y
卷: 463, 期:4, 页:513-522
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Physiology
研究领域[WOS]: Physiology
关键词[WOS]: ISOLATED CARDIAC MYOCYTES ; GUINEA-PIG ; HYDROGEN-PEROXIDE ; CALCIUM EXCHANGE ; NITRIC-OXIDE ; HIPPOCAMPAL-NEURONS ; HEART-CELLS ; INJURY ; INHIBITION ; ANOXIA
英文摘要:

The increases in persistent sodium currents (I (Na.P)) and Na+/H+ exchange (NHE) causes intracellular Ca2+ overload. The objective of this study was to determine the contribution of I (Na.P) and NHE on the hypoxia- or acute ischemia-induced increase in the reverse Na+/Ca2+ exchange current (HIR- or AIR-I (NCX)). I (Na.P) and I (NCX) in rabbit ventricular myocytes were recorded during hypoxia or acute ischemia, combination of acidosis (pH values were 6.0 intracellularly and 6.8 extracellularly) and hypoxia, using whole-cell patch-clamp techniques. The results indicate that (1) under hypoxic condition, the augmentation of both HIR-I (NCX) and I (Na.P) was inhibited by TTX (2 to 8 mu M) in a concentration-dependent manner. The inhibitions of I (Na,P) and HIR-I (NCX) reached maximum in the presence of either 4 mu M TTX or 10 mu M KR-32568 (a NHE inhibitor), respectively. The maximal inhibitions of HIR-I (NCX) by 4 mu M TTX and 10 mu M KR-32568 were 72.54% and 16.89%, respectively. (2) Administration of 2 mu M TTX and 10 mu M KR-32568 in either order in the same cells decreased HIR-I (NCX) by 64.83% and 16.94%, respectively. (3) I (Na.P) and the reverse I (NCX) were augmented during acute ischemia. TTX (4 mu M) and KR-32568 (10 mu M) reduced AIR-I (NCX) by 73.39% and 24.13%, respectively. (4) Under normoxic condition, veratridine (20 mu M) significantly increased I (Na.P) and the reverse I (NCX), which was reversed by 4 mu M TTX. In conclusion, during hypoxia or acute ischemia, both increased I (Na.P) and NHE contribute to the HIR- or AIR-I (NCX) with the former playing a major role comparing with the latter.

语种: 英语
所属项目编号: 30870912
项目资助者: National Natural Science Foundation of China
WOS记录号: WOS:000301524000001
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/51426
Appears in Collections:北京大学第一临床医学院_心血管内科_期刊论文

Files in This Item:

There are no files associated with this item.


作者单位: 1.Wuhan Univ Sci & Technol, Coll Med, Cardio Electphysiol Res Lab, Wuhan 430081, Hubei, Peoples R China
2.Peking Univ, First Hosp, Dept Cardiol, Beijing 100871, Peoples R China

Recommended Citation:
Tang, Qiong,Ma, Jihua,Zhang, Peihua,et al. Persistent sodium current and Na+/H+ exchange contributes to the augmentation of the reverse Na+/Ca2+ exchange during hypoxia or acute ischemia in ventricular myocytes[J]. PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY,2012,463(4):513-522.
Service
Recommend this item
Sava as my favorate item
Show this item's statistics
Export Endnote File
Google Scholar
Similar articles in Google Scholar
[Tang, Qiong]'s Articles
[Ma, Jihua]'s Articles
[Zhang, Peihua]'s Articles
CSDL cross search
Similar articles in CSDL Cross Search
[Tang, Qiong]‘s Articles
[Ma, Jihua]‘s Articles
[Zhang, Peihua]‘s Articles
Related Copyright Policies
Null
Social Bookmarking
Add to CiteULike Add to Connotea Add to Del.icio.us Add to Digg Add to Reddit
所有评论 (0)
暂无评论
 
评注功能仅针对注册用户开放,请您登录
您对该条目有什么异议,请填写以下表单,管理员会尽快联系您。
内 容:
Email:  *
单位:
验证码:   刷新
您在IR的使用过程中有什么好的想法或者建议可以反馈给我们。
标 题:
 *
内 容:
Email:  *
验证码:   刷新

Items in IR are protected by copyright, with all rights reserved, unless otherwise indicated.

 

 

Valid XHTML 1.0!
Copyright © 2007-2017  北京大学医学部 - Feedback
Powered by CSpace