| Project/Area Number |
11480003
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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 |
体育学
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| Research Institution | University of Tsukuba |
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Principal Investigator |
MATSUDA Mitsuo University of Tsukuba, Institute of Health and Sport Sciences, Professor, 体育科学系, 教授 (20110702)
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| Co-Investigator(Kenkyū-buntansha) |
MAEDA Seiji University of Tsukuba, Institute of Clinical Medicine, Research Fellow of the Japan Society for the Promotion of Science, 臨床医学系, 日本学術振興会特別研究員
MIYAUCHI Takashi University ofTsukuba, Institute of Clinical Medicine, Assistant Professor, 臨床医学系, 講師 (60222329)
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| Project Period (FY) |
1999 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥14,600,000 (Direct Cost: ¥14,600,000)
Fiscal Year 2001: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2000: ¥5,400,000 (Direct Cost: ¥5,400,000)
Fiscal Year 1999: ¥7,700,000 (Direct Cost: ¥7,700,000)
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| Keywords | endothelin / nitric oxide / exercise / exercise training / vascular endntlielial cell / cross talk / aging / arterial compliance / 水泳トレーニング / 血流再配分 / エンドセリン受容体遮断薬 / 血管伸展性 / 内皮型一酸化窒素合成酵素 / 脱トレーニング |
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| Research Abstract |
The purpose of the present study was to investigate whether the endothelium-derived vasoactive substances (endothelin-1 [ET-1], a potent vasoconstrictor peptide, and nitric oxide [NO], a potent vasodilator substance) participate in the circulatory regulation during exercise. The products of this study are follows. First, by using ET-1 antagonist, we demonstrated that the ET-1-mediated vasoconstriction participates in the exercise-induced redistribution of tissue blood flow, I.e. the decrease of blood flow internal organs and the increase of blood flow active muscles during exercise. Furthermore, it was revealed that an increase of ET-1 production in the kidney during exercise contributes to a decrease of NO production in the kidney. Therefore, in the blood vessels of the internal organs, the increased ET-1 appears to contribute to the exercise-induced redistribution of blood flow by its direct action and by inhibiting the vasodilative action of NO. Second, we demonstrated that the exercise training caused a decrease in ET-1 production and an increase in NO production in both healthy young and older humans. Furthermore, we showed that the gene and protein expression of endothelial NO synthase (eNOS) in the aorta of rat is decreased by aging, and that the expression is increased by exercise training. Third, we examined whether the distensibility and compliance of large arteries, which may be affected by the endothelium-derived vasoactive substances, are altered with an acute exercise and the exercise training of short-duration in humans. We demonstrated that the distensibility of large arteries is elevated during an acute exercise, and that the exercise training of short-duration causes an increase of systemic arterial compliance at rest and during exercise. We propose a possibility that the exercise-induced alteration of endothelial functions might be related to the rapid increase of large arterial distensibility and compliance.
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