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pubmed-article:21716722pubmed:abstractTextAutoantibodies targeting the ?(1)-adrenergic receptor (AAB-?(1)) display agonist-like effects, which may have a pathogenic role in the progression of heart failure. Here, we used the electrophysiological recordings to explore the effects of AAB-?(1)-positive serum from Chinese patients with heart failure on the activity of the peak transient outward potassium current (I(to)) and the end 50 ms steady-state potassium current (I(ss)) in mouse cardiac myocytes. We found that the AAB-?(1)-positive serum had no effect on the activity of I(to), but it produced a decrease in the currents of I(ss). A low concentration of positive serum (1/100) had a small inhibitory effect on I(ss). However, positive serum at 1?:?10, 1?:?20, and 1?:?50 significantly decreased I(ss). The concentration-dependence analysis showed that the EC(50) of AAB-?(1)-positive serum was 1/60.24 and its nH was 2.86. It indicated that the AAB-?(1) could inhibit I(ss) in mouse cardiomyocyte in a concentration-dependent manner.lld:pubmed
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pubmed-article:21716722pubmed:authorpubmed-author:ZhangYunYlld:pubmed
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pubmed-article:21716722pubmed:authorpubmed-author:ZhangWeiWlld:pubmed
pubmed-article:21716722pubmed:authorpubmed-author:LiXiao-DongXDlld:pubmed
pubmed-article:21716722pubmed:authorpubmed-author:WangYuan-yuan...lld:pubmed
pubmed-article:21716722pubmed:authorpubmed-author:WangJian-chun...lld:pubmed
pubmed-article:21716722pubmed:authorpubmed-author:MaZhi-YongZYlld:pubmed
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pubmed-article:21716722pubmed:volume2011lld:pubmed
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pubmed-article:21716722pubmed:articleTitleSerum positive for the autoantibody against the ?(1)-adrenoceptor from Chinese patients with congestive heart failure decreases I(ss) in mouse cardiac myocytes.lld:pubmed
pubmed-article:21716722pubmed:affiliationKey Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Public Health, Jinan 250012, China.lld:pubmed
pubmed-article:21716722pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:21716722pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed