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In the hypertrophied heart, however, these channels are re-expressed and generate a hyperpolarization-activated, nonselective cation current (I-h), which evidence suggests may increase susceptibility to arrhythmia. To test this hypothesis, we generated and analyzed transgenic mice overexpressing HCN2 specifically in their hearts (HCN2-Tg). Under physiological conditions. HCN2-Tg mice exhibited no discernible abnormalities. After the application of isoproterenol (ISO), however, ECG recordings from HCN2-Tg mice showed intermittent atrioventricular dissociation followed by idioventricular rhythm. Consistent with this observation, 0.31 mu mol/L ISO-induced spontaneous action potentials (SAPs) in 76% of HCN2-Tg ventricular myocytes. In the remaining 24%. ISO significantly depolarized the resting membrane potential (RMP). and the late repolarization phase of evoked action potentials (APs) was significantly longer than in WT myocytes. 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Ectopic automaticity induced in ventricular myocytes by transgenic overexpression of HCN2
http://hdl.handle.net/10091/00021009
http://hdl.handle.net/10091/000210090317a578-49e3-43de-a400-4c9cdc4eb91d
名前 / ファイル | ライセンス | アクション |
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1-s2.0-S0022282814004313-main.pdf (1.4 MB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2018-10-31 | |||||
タイトル | ||||||
言語 | en | |||||
タイトル | Ectopic automaticity induced in ventricular myocytes by transgenic overexpression of HCN2 | |||||
言語 | ||||||
言語 | eng | |||||
DOI | ||||||
識別子タイプ | DOI | |||||
関連識別子 | https://doi.org/10.1016/j.yjmcc.2014.12.019 | |||||
関連名称 | 10.1016/j.yjmcc.2014.12.019 | |||||
キーワード | ||||||
主題 | HCN2, Arrhythmia, Ion channel, Cardiomyocyte, Electrophysiology | |||||
資源タイプ | ||||||
資源 | http://purl.org/coar/resource_type/c_6501 | |||||
タイプ | journal article | |||||
著者 |
Oshita, Kensuke
× Oshita, Kensuke× Ltoh, Masayuki× Hirashima, Shingo× Kuwabara, Yoshihiro× Lshihara, Keiko× Kuwahara, Koichiro× Nakao, Kazuwa× Kimura, Takeshi× Nakamura, Kei-ichiro× Ushijima, Kazuo× Takano, Makoto |
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信州大学研究者総覧へのリンク | ||||||
氏名 | Kuwahara, Koichiro | |||||
URL | http://soar-rd.shinshu-u.ac.jp/profile/ja.HVchWCcp.html | |||||
出版者 | ||||||
出版者 | ELSEVIER SCI LTD | |||||
引用 | ||||||
内容記述タイプ | Other | |||||
内容記述 | JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY. 80: 81-89(2015) | |||||
書誌情報 |
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY 巻 80, p. 81-89, 発行日 2015-01-03 |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Hyperpolarization-activated cyclic nucleotide-gated channels (HCNs) are expressed in the ventricles of fetal hearts but are normally down-regulated as development progresses. In the hypertrophied heart, however, these channels are re-expressed and generate a hyperpolarization-activated, nonselective cation current (Ih), which evidence suggests may increase susceptibility to arrhythmia. To test this hypothesis, we generated and analyzed transgenic mice overexpressing HCN2 specifically in their hearts (HCN2-Tg). Under physiological conditions, HCN2-Tg mice exhibited no discernible abnormalities. After the application of isoproterenol (ISO), however, ECG recordings from HCN2-Tg mice showed intermittent atrioventricular dissociation followed by idioventricular rhythm. Consistent with this observation, 0.3 μmol/L ISO-induced spontaneous action potentials (SAPs) in 76% of HCN2-Tg ventricular myocytes. In the remaining 24%, ISO significantly depolarized the resting membrane potential (RMP), and the late repolarization phase of evoked action potentials (APs) was significantly longer than in WT myocytes. Analysis of membrane currents revealed that these differences are attributable to the Ih tail current. These findings suggest HCN2 channel activity reduces the repolarization reserve of the ventricular action potential and increases ectopic automaticity under pathological conditions such as excessive β-adrenergic stimulation. | |||||
資源タイプ(コンテンツの種類) | ||||||
内容記述タイプ | Other | |||||
内容記述 | Article | |||||
ISSN | ||||||
収録物識別子タイプ | PISSN | |||||
収録物識別子 | 0022-2828 | |||||
書誌レコードID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AA00702819 | |||||
PubMed | ||||||
識別子タイプ | PMID | |||||
関連識別子 | https://www.ncbi.nlm.nih.gov/pubmed/25562801 | |||||
関連名称 | 25562801 | |||||
権利 | ||||||
権利情報 | © 2015 The Authors. Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/) | |||||
出版タイプ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
WoS | ||||||
表示名 | Web of Science | |||||
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