| Angiotensin type 1 receptor blockade prevents endocardial dysfunction of rapidly paced atria in rats. | |
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MedLine Citation:
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PMID: 17907100 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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INTRODUCTION: Atrial fibrillation (AF) per se causes atrial endocardial dysfunction leading to local coagulation imbalance on the internal surface of the atrium, which contributes to thrombus formation in the fibrillating left atrium. MATERIALS AND METHODS: To test a hypothesis that blockade of angiotensin II type 1 receptor (AT1-receptor) prevents the endocardial dysfunction by AF, we examined the effects of olmesartan on the expression of tissue factor pathway inhibitor (TFPI), thrombomodulin (TM), endothelial nitric oxide synthase (eNOS) and plasminogen activator inhibitor-1 (PAI-1) in the endocardium of the rapidly paced rat atria. RESULTS: Rapid pacing induced a significant decrease in TFPI, TM and eNOS and an increase in PAI-1 protein in the left atrium. Pre-administration of low-dose olmesartan significantly prevented the down-regulation of TFPI, TM and eNOS and also attenuated the up-regulation of PAI-1. Immunohistochemistry identified these changes predominantly in the atrial endocardium. While the drug was without any effect on mRNA levels of TFPI, TM and eNOS, there was a significant decrease in its PAI-1 mRNA expression. CONCLUSIONS: AT1-receptor blocker could partially prevent the atrial endocardial dysfunction by rapid atrial pacing, which would provide one theoretical basis for beneficial effects for stroke prevention in AF. |
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Authors:
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Takeshi Yamashita; Akiko Sekiguchi; Takeshi Kato; Takayuki Tsuneda; Yu-ki Iwasaki; Kouichi Sagara; Hiroyuki Iinuma; Hitoshi Sawada; Tadanori Aizawa |
Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Journal of the renin-angiotensin-aldosterone system : JRAAS Volume: 8 ISSN: 1470-3203 ISO Abbreviation: J Renin Angiotensin Aldosterone Syst Publication Date: 2007 Sep |
Date Detail:
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Created Date: 2007-10-01 Completed Date: 2008-01-02 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 100971636 Medline TA: J Renin Angiotensin Aldosterone Syst Country: England |
Other Details:
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Languages: eng Pagination: 127-32 Citation Subset: IM |
Affiliation:
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The Cardiovascular Institute, Roppongi 7-3-10, Tokyo 106-0032, Japan. yamt-tky@umin.ac.jp |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Angiotensin II Type 1 Receptor Blockers
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administration & dosage,
pharmacology* Animals Atrial Fibrillation / complications*, etiology Cardiac Pacing, Artificial / methods Dose-Response Relationship, Drug Down-Regulation / drug effects Endocardium* / physiopathology Heart Atria Heart Diseases / etiology*, physiopathology, prevention & control* Imidazoles / administration & dosage, pharmacology* Immunohistochemistry Lipoproteins / genetics, metabolism Myocardium / metabolism Nitric Oxide Synthase Type III / genetics, metabolism Plasminogen Activator Inhibitor 1 / genetics, metabolism RNA, Messenger / metabolism Rats Rats, Sprague-Dawley Tetrazoles / administration & dosage, pharmacology* Thrombomodulin / genetics, metabolism Up-Regulation / drug effects |
| Chemical | |
Reg. No./Substance:
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0/Angiotensin II Type 1 Receptor Blockers; 0/Imidazoles; 0/Lipoproteins; 0/Plasminogen Activator Inhibitor 1; 0/RNA, Messenger; 0/Tetrazoles; 0/Thrombomodulin; 0/lipoprotein-associated coagulation inhibitor; 0/olmesartan; EC 1.14.13.39/Nitric Oxide Synthase Type III |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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