| Project/Area Number |
13672405
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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 |
応用薬理学・医療系薬学
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| Research Institution | Kinki University |
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Principal Investigator |
KAWABATA Atsufumi Kinki University, Pharmaceutical Sciences, Associate Professor, 薬学部, 助教授 (20177728)
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| Co-Investigator(Kenkyū-buntansha) |
KURODA Ryotaro Kinki University, Pharmaceutical Sciences(retired in March,2003), Professor, 薬学部(H15年3月退職), 教授 (10161803)
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| Project Period (FY) |
2001 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2003: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2002: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2001: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | PAR-2 / blood vessel / endotoxin / inflammation / protease / sensory neuron / pain / salivary gland / PAR / 内臓痛 / 肺上皮細胞 / プロスタグランジン / EDHF / 耳下腺 / Fos / 唾液 / 血圧 |
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| Research Abstract |
The protease-activated receptor(PAR), a G protein-coupled receptor family consists of 4 members, and modulates a variety of physiological functions upon activation in response to inflammation, tissue injury and hemorrhage. The present study investigated the roles and changes of PARs, particularly PAR-2, in acute inflammation.
We first studied changes of sensitivity of PAR-2 present in the salivary glands in mice treated with lipopolysaocharide, and found that PAR-2 might be tonically activated and desensitized by endogenous PAR-2 activators under systemic inflammatory conditions. Endogenous PAR activators including thrombin, factors VII and X, mast cell tryptase might become activated and/or accessible to tissues in septic shock. Vasodilation by these enzymes via PAR activation might contribute to development of hypotension caused by septic shock. In this context, we examined the mechanisms underlying the vascular contraction and relaxation caused by PAR activation. We then investigated roles of PARs, known to be present in capsaicin-sensitive sensory neurons, in inflammatory visceral pain and parotitis-related pain. Our data provide novel evidence that PARs, particularly PAR-2,is involved in inflammation and related pain, circulatory disturbance, etc.
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