| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
|
|---|
| 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.
|
