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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6
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pubmed:dateCreated |
2004-8-10
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pubmed:abstractText |
The blockade of beta-adrenergic receptors reduces both mortality and morbidity in patients with chronic heart failure, but the cellular mechanism remains unclear. Celiprolol, a selective beta(1)-blocker, was reported to stimulate the expression of endothelial NO synthase (eNOS) in the heart, and NO levels have been demonstrated to be related to myocardial hypertrophy and heart failure. Thus, we aimed to clarify whether celiprolol attenuates both myocardial hypertrophy and heart failure via the NO-signal pathway.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adrenergic beta-1 Receptor...,
http://linkedlifedata.com/resource/pubmed/chemical/Adrenergic beta-Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Celiprolol,
http://linkedlifedata.com/resource/pubmed/chemical/Isoproterenol,
http://linkedlifedata.com/resource/pubmed/chemical/NG-Nitroarginine Methyl Ester,
http://linkedlifedata.com/resource/pubmed/chemical/Natriuretic Peptide, Brain,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type II,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type III,
http://linkedlifedata.com/resource/pubmed/chemical/Nos3 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Nos3 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Phenylephrine,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Vasodilator Agents
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1524-4539
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pubmed:author |
pubmed-author:AsakuraMasanoriM,
pubmed-author:AsanoYoshihiroY,
pubmed-author:AsanumaHiroshiH,
pubmed-author:HoriMasatsuguM,
pubmed-author:KimJiyoongJ,
pubmed-author:KitakazeMasafumiM,
pubmed-author:KitamuraSoichiroS,
pubmed-author:LiaoYulinY,
pubmed-author:MinaminoTetsuoT,
pubmed-author:OgaiAkikoA,
pubmed-author:SanadaShojiS,
pubmed-author:ShintaniYasunoriY,
pubmed-author:TakashimaSeijiS,
pubmed-author:TomoikeHitonobuH
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pubmed:issnType |
Electronic
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pubmed:day |
10
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pubmed:volume |
110
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
692-9
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:15262839-Adrenergic beta-1 Receptor Antagonists,
pubmed-meshheading:15262839-Adrenergic beta-Antagonists,
pubmed-meshheading:15262839-Animals,
pubmed-meshheading:15262839-Cardiomegaly,
pubmed-meshheading:15262839-Celiprolol,
pubmed-meshheading:15262839-Cells, Cultured,
pubmed-meshheading:15262839-Disease Progression,
pubmed-meshheading:15262839-Drug Evaluation, Preclinical,
pubmed-meshheading:15262839-Enzyme Induction,
pubmed-meshheading:15262839-Fibrosis,
pubmed-meshheading:15262839-Gene Expression Regulation,
pubmed-meshheading:15262839-Heart Failure,
pubmed-meshheading:15262839-Hypertrophy,
pubmed-meshheading:15262839-Isoproterenol,
pubmed-meshheading:15262839-Male,
pubmed-meshheading:15262839-Mice,
pubmed-meshheading:15262839-Mice, Inbred C57BL,
pubmed-meshheading:15262839-Myocardium,
pubmed-meshheading:15262839-Myocytes, Cardiac,
pubmed-meshheading:15262839-NG-Nitroarginine Methyl Ester,
pubmed-meshheading:15262839-Natriuretic Peptide, Brain,
pubmed-meshheading:15262839-Nitric Oxide,
pubmed-meshheading:15262839-Nitric Oxide Synthase,
pubmed-meshheading:15262839-Nitric Oxide Synthase Type II,
pubmed-meshheading:15262839-Nitric Oxide Synthase Type III,
pubmed-meshheading:15262839-Phenylephrine,
pubmed-meshheading:15262839-Pressure,
pubmed-meshheading:15262839-RNA, Messenger,
pubmed-meshheading:15262839-Rats,
pubmed-meshheading:15262839-Transcription, Genetic,
pubmed-meshheading:15262839-Vasodilator Agents
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pubmed:year |
2004
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pubmed:articleTitle |
Celiprolol, a vasodilatory beta-blocker, inhibits pressure overload-induced cardiac hypertrophy and prevents the transition to heart failure via nitric oxide-dependent mechanisms in mice.
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pubmed:affiliation |
Department of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine, Osaka, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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