| Project/Area Number |
04670571
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | NATIIONAL CARDIOVASCULAR CENTER RESEARCH INSTITUTE |
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Principal Investigator |
MATSUDA Hisao NATIIONAL CARDIOVASCULAR CENTER RESEARCH INSTITUTE, DEPARTMENT OF CARDIOVASCULAR DYNAMICS, REGULAR RESEARCH STAFF, 循環動態機能部, 室員 (30229489)
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| Co-Investigator(Kenkyū-buntansha) |
MIYATAKE Kunio NATIIONAL CARDIOVASCULAR CENTER, CARDIOLOGY DIVISION OF MEDICINE, DIRECTOR, 内科心臓部門, 部長
BEPPU Shintaro NATIIONAL CARDIOVASCULAR CENTER RESEARCH INSTITUTE, DEPARTMENT OF CARDIOVASCULAR, 循環動態機能部, 室長 (40113500)
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| Project Period (FY) |
1992 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1993: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1992: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | Endothelium / Perivascular Nerve Stimulation / Endothelin / Nitric Oxide / Eicosanoid / Perivascular Nerve Stimulatioan / Endothelina / Periarterial Nerve Stimulation |
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| Research Abstract |
The present study attempted to examine the regulatory mechanism of vascular smooth muscular tone based on neuroeffector-endothelial interaction, employing isolated vascular tissue with the use of perivascular nerve stimulation (PNS). As a result, it is indicated that nitric oxide (NO)might be released on PNS and modulate autonomic adrenergic neurotransmision in guinea pig arteries (pulmonary and iliac artery). In guinea pig pulmonary artery, sensory neuropeptides (calcitonin gene-related peptide and substance P) are also indicated to be released on PNS and participate in modulation of autonomic adrenergic neurotransmission.
The mechanism of PNS-induced release of NO was further investigated and it was indicated that noradrenaline released on PNS could act onendothelium resulting in release of NO.Sensory neuropeptides released on PNS could also participate in endothelial NO release. Additionally, a dilator nerve relasing NO was indicated in guinea pig pulmonary artery. With respect to the mode of endothelin (ET)-1 action, the invivo investigation was done. As a result, secondary release of cyclo-oxygenase-generated eicosanoid(s), mainly thromboxane A_2 was suggested to be responsible for the pressor response of ET-1. The interactions between ET-1 and other vasoactive autacoids were examined employing cultured endothelial cells and increase in the level of prostacyclin (6-keto-prostaglandin F_<1alpha>) was observed in the culture media after administration of endothelin-1. The interactions between other autacoids are being investigated.
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