Item type |
学術雑誌論文 / Journal Article(1) |
公開日 |
2014-06-12 |
タイトル |
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タイトル |
β(2)-Adrenergic and M(2)-muscarinic receptors decrease basal t-tubular L-type Ca2+ channel activity and suppress ventricular contractility in heart failure |
言語 |
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言語 |
eng |
DOI |
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関連識別子 |
https://doi.org/10.1016/j.ejphar.2013.12.037 |
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関連名称 |
10.1016/j.ejphar.2013.12.037 |
キーワード |
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主題 |
Heart failure, L-type Ca2+ channels, Protein phosphatase, beta(2)-adrenergic receptor, M-2-muscarinic receptor, A(1)-adenosine receptor |
資源タイプ |
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資源 |
http://purl.org/coar/resource_type/c_6501 |
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タイプ |
journal article |
著者 |
Kashihara, Toshihide
Hirose, Masamichi
Shimojo, Hisashi
Nakada, Tsutomu
Gomi, Simmon
Hongo, Minoru
Yamada, Mitsuhiko
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信州大学研究者総覧へのリンク |
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氏名 |
Nakada, Tsutomu |
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URL |
http://soar-rd.shinshu-u.ac.jp/profile/ja.OVkhuNkh.html |
信州大学研究者総覧へのリンク |
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氏名 |
Yamada, Mitsuhiko |
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URL |
http://soar-rd.shinshu-u.ac.jp/profile/ja.jhSCupca.html |
出版者 |
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出版者 |
ELSEVIER SCIENCE BV |
引用 |
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内容記述 |
EUROPEAN JOURNAL OF PHARMACOLOGY. 724:122-131 (2014) |
書誌情報 |
EUROPEAN JOURNAL OF PHARMACOLOGY
巻 724,
p. 122-131,
発行日 2014-02-05
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抄録 |
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内容記述 |
L-Lype Ca2+ channels (LTCC) play a crucial role in cardiac excitation-contraction coupling. We previously found that in failing ventricular myocytes of mice chronically treated with isoproterenol, basal t-tubular (TT) LTCC activity was halved by activation of protein phosphatase (PP)2A whereas basal surface sarcolemmal (SS) LTCC activity was doubled by inhibition of PP1. Interestingly, chronic treatment of these mice with pertussis toxin almost completely normalized TT and SS LTCC densities and cardiac contractility. In the present study, we therefore sought to identify the G(i/o) protein coupled receptors in cardiac myocytes (i.e. beta(2)-adrenergic, M-2-muscarinic and A(1)-adenosine receptors) that are responsible for these abnormalities in heart failure by chronically administrating mice a selective antagonist of each receptor (ICI118,551, atropine and 8-cyclopentyl-1,3-dipropilxanthine (DPCPX), respectively) with isoproterenol. Compared with mice treated with isoproterenol alone, mice treated with isoproterenol plus ICI118,551 or atropine, but not DPCPX showed significantly lower lung weight/tibial length, higher fractional shortening, lower left ventricular end-diastolic pressure and higher dP/dt(max) and dP/dt(min). In addition, ventricular myocytes of mice treated with isoproterenol plus ICI118,551 or atropine, but not DPCPX exhibited significantly higher TT and lower SS LTCC current densities than those of mice treated with isoproterenol alone due to normalization of the PP activities. These results indicate that beta(2)-adrenergic, M-2-muscarinic, but not A(1)-adenosine receptors contribute to reduced ventricular contractility at least partially by decreasing basal TT LTCC activity in heart failure. Therefore, antagonists of beta(2)-alrenergic and/or M-2-muscarinic receptors can be good adjuncts to beta(1)-adrenergic receptor antagonists in the treatment of heart failure. |
資源タイプ(コンテンツの種類) |
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ISSN |
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収録物識別子タイプ |
PISSN |
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収録物識別子 |
0014-2999 |
書誌レコードID |
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収録物識別子タイプ |
NCID |
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収録物識別子 |
AA00639687 |
PubMed |
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識別子タイプ |
PMID |
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関連識別子 |
https://pubmed.ncbi.nlm.nih.gov/24389135 |
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関連名称 |
24389135 |
権利 |
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権利情報 |
Copyright© 2013 Elsevier B.V. |
出版タイプ |
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出版タイプ |
AM |
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出版タイプResource |
http://purl.org/coar/version/c_ab4af688f83e57aa |
WoS |
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URL |
http://gateway.isiknowledge.com/gateway/Gateway.cgi?&GWVersion=2&SrcAuth=ShinshuUniv&SrcApp=ShinshuUniv&DestLinkType=FullRecord&DestApp=WOS&KeyUT=000331140500015 |