2013 Fiscal Year Final Research Report
Role of protease-activated receptor 2 in metabolic syndrome
| Project/Area Number |
23590315
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General pharmacology
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| Research Institution | Mukogawa Women's University |
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Principal Investigator |
KAGOTA Satomi 武庫川女子大学, 薬学部, 准教授 (00291807)
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| Co-Investigator(Renkei-kenkyūsha) |
MARUYAMA Kana 武庫川女子大学, 薬学部, 助手 (20611396)
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| Project Period (FY) |
2011 – 2013
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| Keywords | 血管拡張機能 / メタボリックシンドローム / PAR-2 / 一酸化窒素 |
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| Research Abstract |
Metabolic syndrome (MetS) is characterized by accumulation of atherosclerotic risk. Increased visceral adiposity is attributed to the development of cardiovascular complications in the syndrome via overproduction of inflammatory factors released from adipocytes. However, the role of protease-activated receptor 2 (PAR2) in vascular responsiveness in MetS is not fully understood. Therefore, we studied changes in PAR2-mediated vasodilation using an animal model of MetS.
Our study demonstrates that PAR2-mediated vasodilation is preserved even though nitric oxide (NO)-mediated vasodilation by other agonists is impaired in arteries of MetS rats. Enhancement of endothelial NO synthase may play important role in the preservation of PAR2-mediated vasodilation. Furthermore, we propose that perivascular adipose tissue wrapped around the blood vessel enhances NO-mediated vasodilation under pathophysiological conditions to compensate for impaired vasodilation in MetS.
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[Presentation] Chronic administration of tempol protects impaired coronary vasodilation in metabolic syndrome model rats, SHRSP.Z-Lepr^fa/IzmDmcr rats2012
Author(s)
Kagota S., Maruyama K., Fukushima K., Umetani K., Tada Y., Wakuda H., Kunitomo M., Nakamura K., Shinozuka K.
Organizer
24th ISH2012
Place of Presentation
Sydney, Australia
Year and Date
2012-10-03
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