2011 Fiscal Year Final Research Report
Glucocorticoid-induced vascular endothelial dysfunction through activation of mineralcorticoid receptor
| Project/Area Number |
21590955
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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 | The University of Tokushima |
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Principal Investigator |
AKAIKE Masashi 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 教授 (90271080)
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| Co-Investigator(Kenkyū-buntansha) |
IWASE Takshi 徳島大学, 病院, 助教 (10403718)
AIHARA Ken-ichi 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 講師 (70372711)
YAGI Shusuke 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 助教 (00507650)
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| Project Period (FY) |
2009 – 2011
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| Keywords | グルココルチコイド / ミネラルコルチコイド / 血管内皮細胞 / 酸化ストレス / 一酸化窒素 |
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| Research Abstract |
Hydrocortisone and methylprednisolone significantly increased glucocorticoid transcriptional activity and production of superoxide, and decreased expression and activation of endothelial nitric oxide synthase in cultured vascular endothelial cells. Thease effects were suppressed by spironolactone and eplerenone. Glucocorticoid excess enhanced oxidative stress and attenuated nitric oxide production through activation of mineralcorticoid recptor, leading to vascular endothelial dysfunction.
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[Journal Article] Heparin Cofactor II protects against angiotensin II-induced cardiac remodeling via attenuation of oxidative stress in mice2010
Author(s)
Sumitomo-Ueda Y, Aihara K, Ise T, Yoshida S, Ikeda Y, Uemoto R, Yagi S, Iwase T, Hirata Y, Akaike M, et al
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Journal Title
Hypertension
Volume: 56(3)
Pages: 430-436
DOI
Peer Reviewed
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