| Project/Area Number |
24591104
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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 |
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) |
UCHIWA Hiroki 久留米大学, 医学部, 助教 (30624506)
KAJIMOTO Hidemi 久留米大学, 医学部, 助教 (50349700)
AOKI Yuji 久留米大学, 医学部, 助教 (80597419)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 血圧変動 / 高血圧 / 心肥大 / 線維化 / 炎症 / 心臓リモデリング / 血管リモデリング |
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| Outline of Final Research Achievements |
The aim of this study was to determine the key molecule of aggravation of hypertensive organ damage by large blood pressure (BP) variability. First, using a model of a combination of hypertension and large BP variability, large BP variability activated mineralocortioid receptor (MR), Rac, and PAK in medial smooth muscle of the intramyocardial arterioles. A sub-depressure dose of selective MR inhibitor, eplerenone prevented chronic inflammatory changes, cardiac hypertrophy, myocardial fibrosis, and LV systolic dysfunction. Accordingly, it was suggested that the Rac-PAK-MR system plays a role in the aggravation of the large BP variability-induced aggravation of hypertensive organ damages. Currently, further investigation using genetically engineered mice is on-going to determine the causal relation between MR system and large BP variability-induced aggravation of hypertensive organ damages.
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