| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Outline of Final Research Achievements |
We have shown previously that sympathoexcitation by brain oxidative stress mediates arterial pressure elevation in hypertension, and also shown that aldosterone-mineralocorticoid receptor (MR) activation mediates oxidative stress-induced cardiac and renal dysfunction. Then, we hypothesized that brain MR activation could mediate arterial pressure elevation through brain oxidative stress-induced sympathoexcitation. We used high-salt-loaded Dahl-salt-sensitive rats, high-fat-loaded-Sprague-Dawley rats and Dahl-S.Z-Lepr(fa)/Lepr(fa)). In these rats, mRNA expression of Sgk-1 and PAI-1 in the hypothalamus was significantly enhanced, which suggested MR activation. Moreover, chronic intracerebroventricular eplerenone significantly reduced sympathetic nerve activity and arterial pressure. In conclusion, brain aldosterone-MR activation through btsin oxidative stress-induced sympathoexcitation can be a possible pathogenic background of hypertension in metabolic syndrome.
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