Document Detail


Angiotensin type 1 receptor blockade prevents endocardial dysfunction of rapidly paced atria in rats.
MedLine Citation:
PMID:  17907100     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Takeshi Yamashita; Akiko Sekiguchi; Takeshi Kato; Takayuki Tsuneda; Yu-ki Iwasaki; Kouichi Sagara; Hiroyuki Iinuma; Hitoshi Sawada; Tadanori Aizawa
Publication Detail:
Type:  Journal Article    
Journal Detail:
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:
Created Date:  2007-10-01     Completed Date:  2008-01-02     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100971636     Medline TA:  J Renin Angiotensin Aldosterone Syst     Country:  England    
Other Details:
Languages:  eng     Pagination:  127-32     Citation Subset:  IM    
Affiliation:
The Cardiovascular Institute, Roppongi 7-3-10, Tokyo 106-0032, Japan. yamt-tky@umin.ac.jp
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MeSH Terms
Descriptor/Qualifier:
Angiotensin II Type 1 Receptor Blockers / 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:
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

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