| Project/Area Number |
07670829
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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 | NATIONAL CARDIOVASCULAR CENTER RESEARCH INSTITUTE |
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Principal Investigator |
MATSUDA Hisao NATIONAL CARDIOVASCULAR CENTER RESEARCH INSTITUTE,DEPARTMENT OF CARDIOVASCULAR DYNAMICS,RESEARCH INSTITUTE,DEPARTMENT OF CARDIOVASCULAR DYNAMICS,RESEARCH STAFF, 循環動態機能部, 室員 (30229489)
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| Co-Investigator(Kenkyū-buntansha) |
MIYATAKE Kunio NATIONAL CARDIOVASCULAR CENTER,CARDIOLOGY DIVISION OF MEDICINE,DIRECTOR, 内科心臓部門, 部長
UEMATSU Masaaki NATIONAL CARDIOVASCULAR CENTER RESEARCH INSTITUTE,DEPARTMENT OF CARDIOVASCULAR D, 循環動態機能部, 室長 (00270728)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1996: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1995: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | JNJURED VESSELS / NEUROEFFECTOR-ENDOTHELIAL INTERACTION / ADRENERGIC CONTRACTION / NITRIC OXIDE / 15-HYDROPEROXYEICOSATETRAENOIC ACID / SENSORY NEUROPEPTIDES / ENDOTHELIN / ENDOTHELIAL THICKENING / バルーン・カテーテル / 血小板活性化因子 / 炎症性サイトカイン / 15-リポキシゲナーゼ / カルシトニン遺伝子関連ペプチド / substance P / アドレナリン作動性収縮反応 |
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| Research Abstract |
This study investigate (1) pharmaco-physiological vasoactive properties of the autacoids possibly acting in injured vessels, and (2) altered adrenergic neurotransmission in these vessels.
With respect to the former part, vasoactive properties of 15-hydroperoxyeicosatetraenoic acid and sensory neuropeptides were studied in relation to endothelial function. As a result, 15-hydroperoxyeicosatetraenoic acid induced both endothelium-dependent vasorelaxation and vasoconstriction which were dependent upon the concentration and the source of the studied vessels. Additionally, sensory neuropeptides, other principal mediators of neuroeffector-endothelial interaction, also showed different modes of vasorelaxation, endothelial nitric oxide-mediated or direct vasorelaxation, which were dependent upon the preparations, arteries or veins. Moreover, this study investigated the effects of endothelins on vascular adrenergic contraction. Endothelins augmented vascular adrenergic contraction via ET_A recep
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tors.
The latter part of the present study investigated altered modulation of adrenergic contraction (AC) in injured muscular artery. Microballoon-injured guinea pig femoral artery (FA) served as material. Nitric oxide synthetase inhibitor significantly augmented AC in both control and injured FA.The degree of the augmentation was significantly attenuated in injured FA,compared with control FA.And so was acetylcholine-induced relaxation after noradrenaline precontraction. Morphologically, progressive endothelial thickening was observed in injured FA.These results indicate that attenuated inhibition of AC with nitric oxide, accompanied by endothelial thickening, could increase vascular tone in injured muscular artery. To further elucidate the mechanism of altered neuroeffector-endothelial interaction in injured artery, effects of platelet-activating factor on vascular AC was studied and this factor was shown to sugment AC via cyclo-oxygenase-generated eicosanoid (s) in an endothelium-dependent manner. Effects of proinflammatory cytokines are also being studied. Less
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