1991 Fiscal Year Final Research Report Summary
The role of phosphatidylinosides-Ca^<2+> system in asthma attack
| Project/Area Number |
02454242
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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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 | Nagoya University |
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Principal Investigator |
TAKAGI Kenzo Nagoya Univ. School of Med., assistant professor, 医学部, 講師 (50093050)
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| Co-Investigator(Kenkyū-buntansha) |
BABA Kenji Aichi Medical University assistant professor, 医学部, 講師 (80211499)
YAMAKI Kenichi Nagoya Univ. School of Med. Assistant, 医学部, 助手 (20182420)
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| Project Period (FY) |
1990 – 1991
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| Keywords | Asthma attack / Phosphatidylinosides / GTP-binding protein / Phospholipase A2 / Protein kinase C / Neuropeptide / Ca channel / Histamine |
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| Research Abstract |
To elucidate the functions of phosphatidylinosides-Ca^<2+> system in asthma attack in patients with bronchial asthma, and physiological, biochemical and pharmacological approaches were performed in this study. In this study using swine tracheal smooth muscle, it was found that phorbol ester which activated protein kinase C, evoked large increases of Ca influx even at small membrane depolarization by contractile agonists that function through receptor activations. It is known that contractile agonists through receptor activations stimulate inositol phospholipid metabolisms in airway smooth muscle cells, resulting in the production of inositol trisphosphate and diacylglycerol which activates protein kinase C. Thus, it is concluded that the responses to slower concentrations of histamine in the presence of the three agonists (PGF, carbachol and serotonin) is mainly dependent on the influx of external Ca and that the agonists-induced activaton of protein kinase C as well as membrane depolarization may be responsible for the increase of the histamine-induced Ca influx, eventually enhancing the histamine contractions.
In addition, we showed that both forms of PACAP tested may act as novel potent relaxants on tracheal smooth muscle by raising tissue cyclic AMP levels and membrane-binding phospholipase A2 activity of PMN would thus appea to be regulated directly by GTP-binding protein.
We should try on next steps to elucidate the functions of inositol triphosphate-Ca^<2+> system in bronchial asthma.
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[Publications] Miyatake,H.,Taki,F.,Taniguchi,H.,Suzuki,R.,Takagi,K.,Satake,T.: "Erythromycin reduces the severity of bronchial hyperresponsiveness in asthma" Chest. 99. 670-673 (1991)
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[Publications] Baba,K.,Ishikawa,M.,Mori,M.,Yamada,K.,Mizuno,K.,Watanabe,T.: "Advances in Asthmology 1990(分担Contractile agonistsーInduced Potentiation of the Responses to Histamine in the GuineaーPig Tracheal Smooth Muscle)" Excerpta Medica, 611(497-500) (1991)
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[Publications] Takagi,K.,Ogawa,K.,Tanaka,H.,Satake,T.,Watanabe,Y.,Chijiwa,T.,Hidaka,H.: "Advances in Seconol Messenger and Phosphoprotein Research volume25 The Biology of Cyclic Nucleotide Phosphodiesterase(分担Relaxant Effects of Various Xanthine Derivatives Relationship to Cyclic Nucleotide Phosphodiesterase Inhibition)" Raven Press, 429(353-362) (1992)
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