| Project/Area Number |
04670473
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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 |
Respiratory organ internal medicine
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| Research Institution | KUMAMOTO UNIVERSITY |
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Principal Investigator |
KOHROGI Hirotsugu Kumamoto University, University Hospital, Instructor, 医学部・附属病院, 助手 (00178237)
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| Co-Investigator(Kenkyū-buntansha) |
KAWANO Osamu Kumamoto University, School of Medicine, Instructor, 医学部, 助手 (40253728)
ANDO Masayuki Kumamoto University, School of Medicine, Professor, 医学部, 教授 (00040204)
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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 |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1993: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1992: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | cough / tachykinins / substance P / asthma / immune response / prostaglandin / leukotriene / tetrodotoxin / チキキニン / ニュートラルエンドペプチダーゼ |
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| Research Abstract |
We have reported that inhibition of neutral endopeptidase potentiates bronchial contraction induced by immune response, leukotriene C_4 and serotonin in guinea pig bronchus. Because neutral endopeptidase effectively cleaves tachykinins, these results suggest that immune response, as a model of airway inflammation, causes release of tachykinins from the bronchus.
In this study, we found that tachykinin antagonist inhibits the potentiation of the contraction induced by neutral endopeptidase inhibitor. So, we confirmed the release of tachykinins in immune response in guinea pig bronchus. Furthermore, we found that neutral endopeptidase inhibitor potentiates prostaglandin F_2a#-induced bronchial contraction, and that the potentiation is blocked by tachykinin antagonist. These results suggest that prostaglandin F_2a# also stimulates release of tachykinins in the guinea pig bronchus. The potentiation of the bronchial contraction was not inhibited by tetrodotoxin. Because tetrodotoxin inhibits nerve conduction, we speculates that chemical mediators released by immune response including prostaglandin F_2a# stimulate directly on nerve ending to release tachykinins without stimulating axon reflex.
We have previously reported that tachykinins stimulates cough response. Our results in the study suggets that inflammation including immune response causes cough response by stimulating release fo tachykinins.
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