| Project/Area Number |
05670413
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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 |
内科学一般
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| Research Institution | University of Tokyo |
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Principal Investigator |
NAKAJIMA Toshiaki University of Tokyo, 2nd Department of Internal Medicine, 医学部(病), 助手 (50227790)
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| Co-Investigator(Kenkyū-buntansha) |
HAZAMA Hisanori 2nd Department of Internal Medicine, 医学部(病), 医員
HAMADA Eiji 2nd Department of Internal Medicine, 医学部(病), 医員
挾間 比左徳 東京大学, 医学部(病), 医員
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| Project Period (FY) |
1993 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1994: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1993: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | Ionic Channel / Tracheal Smooth Muscle / Neurokinin A / Vascular Smooth Muscle / Cl^- Current / Non-Selective Cation Channel / Endothelin / Human Gastric Epithelial Cells / traclea smooth muscle / nearokinin A / Ca^<2+>-actiuated Cl^- current / endotholin / 17β estradiol / Non-selective cation channel / Ionic channel / trachea smooth muscle / neurokinin A / Vascular smooth muscle / Cl^-current / Ca^<2+>-activated K^+current |
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| Research Abstract |
(1) Ca^<2+>-activated Cl^- current in tracheal smooth msucle cells (TSMCs) : We recently reported that neurokinin A causes rapid and sustained depolarization of single TSMCs by two different mechanisms ; (1) initial transient activation of Ca^<2+>-dependent Ca^- current (ICa.L), and (2) sustained inhibition of K^+ currents (Pflugers Arch 1995, in press). The activation of Cl^- current was due to the release of Ca^<2+> from the IP_3-store sites. In addition, we further investigated that the underlying mechanisms of activation of Ca^<2+>-activated Cl^- current in single TSMCs, and found that ICa.L as well as agonist stimulation plays an important role in activating the current, where CICR-sensitive Ca^<2+>-store sites may be involved. Also, it is likely that in guinea -pig TSMCs, IP3 and CICR-sensitive Ca^<2+> store sites may be overlapping.
(2) Mechanism of vasopressin and endothelin-induced calcium influx in aortic smooth msucle cells : The effects of vasopressin and endothelin on cultured rat aortic smooth muscle cells were investigated using the calcium-sensitive dye Indo-1 to measure intracellular Ca^<2+> and the patch clamp-technique. We found that calcium entry elicited by these agents is mediated by the receptoroperated Ca^<2+>-permeable non-selective cation channel in aortic smooth muscle cells (Heart and Vessels, 1995, in press). Also, the present results indicate that endothelin activates Ca^<2+>-dependent K^+ current (IK.Ca) and nonselective cation channel (IN.S.) via the ET_A receptor, and the activation of IK.Ca ismediated presumably by IP_3 and Ca^<2+> from internal store sites, but different mechanisms may be involved in activation of IN.S.via the pertussistoxin insensitive GTP-binding proteins (Circulation (abstract) 1994 : 90 : 200).
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