| Project/Area Number |
06670622
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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 Assisatant Professor, 医学部・附属病院, 講師 (00178237)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAGUCHI Tetsuro Kumamoto University School of Medicine Physician, 医学部・附属病院, 医員
ANDO Masayuki Kumamoto University School of Medicine Professor, 医学部, 教授 (00040204)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1995: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1994: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | cough / tachykinins / substance P / neutral endopeptidase / gastroesophageal reflux / allergy / axon reflex / asthma / ニュートラルエンドペプチダーゼ / 軸束反射 / ニューロキニンA / 接着因子 / 好酸球 |
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| Research Abstract |
In this study, we found that neutral endopeptidase potentiates bronchial contraction induced by immune response in guinea pigs, and that the potentiation is blocked by tachykinin antagonist. So, we confirmed the release of tachykinins in immune response in guinea pig bronchus. Additionally, we also found that neutral endopeptidase potentiates bronchial contraction induced by capsaicin in human bronchus, and that the potentiation is blocked by tachykinin antagonist. Therefore, we speculate that tachykinins exist in the human bronchus and that tachykinins may play an important roles in airway functions.
Furthermore, we found that neutral endopeptidase inhibitor potentiates prostaglandin F_<2alpha>-induced bronchial contraction, and that the potentiation is blocked by tachykinin antagonist. These results suggest that prostaglandin F_<2alpha> 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 reponse including prostaglandin F_<2alpha> stimulate directly on nerve ending to release tachykinins withous stimulating axon reflex. Gastroesophageal reflux is one of diseases that cause or exacerbate cough and asthma. Esophageal stimulation by HCI enhances vascular permeability in the airways, and the response was potentiated by neutral endopeptidase, and blocked by a tachykinin antagonist. So, it suggest that esophageal stimulation causes tachykinin release in the airways
We have previously reported that tachykinins stimulates cough response. Our results in the study suggests that inflammation including immune response and esophageal stimulation cause cough response by stimulating release of tachkinins.
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