2010 Fiscal Year Final Research Report
Hypertension in metabolic syndrome : Mechanism involved in activation of the sympathetic nervous system and therapeutic approach
| Project/Area Number |
19390231
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | Kyushu University |
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Principal Investigator |
HIROOKA Yoshitaka Kyushu University, 大学病院, 講師 (90284497)
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| Co-Investigator(Kenkyū-buntansha) |
KISHI Takuya 九州大学, 大学院・医学研究院, 客員助教 (70423514)
ESHIMA Kenichi 九州大学, 大学病院, 助教 (20444804)
IDE Tomomi 九州大学, 大学病院, 助教 (90380625)
UTSUMI Hideo 九州大学, 先端融合医療レドックスナビ研究拠点, 特任教授 (20101694)
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| Co-Investigator(Renkei-kenkyūsha) |
UTSUMI Hideo 九州大学, 先端融合医療レドックスナビ研究拠点, 特任教授 (20101694)
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| Project Period (FY) |
2007 – 2010
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| Keywords | 血圧 / 交感神経系 / 酸化ストレス / 脳 / 肥満 |
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| Research Abstract |
In the present study, we found that the increased oxidative stress in the brain, particularly in the cardiovascular center in the brainstem, enhanced sympathetic activity thereby causing hypertension in metabolic syndrome. As a major source of reactive oxygen species generation, we found that activation of the angiotensin type 1 receptors and related signaling pathway play an important role in the increased oxidative stress in the brain. In addition, we found that activation of the sympathetic nervous system and endothelial dysfunction occurred in patients with metabolic syndrome. Treatment with angiotensin receptor blockers improved these abnormalities.
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