| Project/Area Number |
21590943
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Kurume University |
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Principal Investigator |
KAI Hisashi 久留米大学, 医学部, 准教授 (60281531)
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| Co-Investigator(Kenkyū-buntansha) |
KAJIMOTO Hidemi 久留米大学, 循環器病研究所, 助教 (50349700)
YASUOKA Suguru 久留米大学, 医学部, 助教 (10461435)
ANAGAWA Takahiro 久留米大学, 医学部, 助教 (00511833)
IKEDA Ayami 久留米大学, 医学部, 助教 (80412500)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 高血圧 / 心筋細胞 / 血管平滑筋 / 遺伝子発現 / 細胞間クロストーク |
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| Research Abstract |
We established a selective and comprehensive gene expression pattern analysis separating the myocardium and vasculature in the heart using the laser microdissection(LMD) method. To investigate the effects of pharmacological intervention at the prehypertensive phase on the development of hypertension, an angiotensin II receptor blocker(ARB) was administered to stroke-prone spontaneously hypertensive rats(SHR-SP) of 4-7 weeks old. SHR-SP with early exposure to ARB showed significantly lower blood pressure at hypertensive stage than those without ARB treatment. Also, the incidence of stroke and the incidence of all cause death were significantly lower in SHR-SP with ARB early exposure than those without ARB. The mRNA expression patterns of the myocardium area and vascular area were being compared separately between SHR-SP with and without ARB early exposure. A rat model of a combination of hypertension and large blood pressure variability(BPV) was created by performing a sino-aortic denervation in spoitaneously hypertensive rats. In normotensive rats, increased BPV induced only limited cardiac hypertrophy and fibrosis. In contrast, large BPV exaggerated cardiac hypertrophy and fibrosis, leading to LV systolic dysfunction in SHR. It was reveled that chronic inflammation of the intramyocardial arterioles elicited the large BPV-induced aggravation of cardiac remodeling. The gene expression profile changes induced specifically by a combination of hypertension and large BPV were being investigated separately in the myocardium area and vascular area.
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