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Research of Ionic Channel and Its Intracellular Signalling Pathwa.

离子通道及其细胞内信号通路的研究。

基本信息

批准号：
05670413
负责人：
NAKAJIMA Toshiaki
金额：
$ 1.28万
依托单位：
University of Tokyo
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1993
资助国家：
日本
起止时间：
1993 至 1994
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-05670413/
关键词：
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

项目摘要

(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).

(1) Ca^<2+>-激活气管平滑肌细胞（TSMCs）中的Cl^-电流：我们最近报道了神经激肽A通过两种不同的机制引起单个TSMCs快速和持续的去极化；(1) Ca^<2+>-依赖Ca^-电流（ICa）的初始瞬态激活。L)和(2)K^+电流的持续抑制（Pflugers Arch 1995, in press）。Cl^-电流的激活是由于Ca^<2+>从IP_3-store位点释放。此外，我们进一步研究了Ca^<2+>-激活单个TSMCs中Cl^-电流的潜在激活机制，发现ICa。L和激动剂刺激在激活电流中起重要作用，其中cicr敏感的Ca^<2+>-存储位点可能参与其中。此外，在豚鼠tsmc中，IP3和cicr敏感的Ca^<2+>存储位点可能重叠。(2)血管加压素和内皮素诱导主动脉平滑肌细胞钙内流的机制：采用钙敏感染料Indo-1测定细胞内Ca^<2+>和膜片钳技术研究血管加压素和内皮素对培养大鼠主动脉平滑肌细胞的影响。我们发现这些药物引起的钙进入是由主动脉平滑肌细胞中受体操作的Ca^<2+>-渗透性非选择性阳离子通道介导的（心脏和血管，1995，出版）。内皮素通过ET_A受体激活Ca^<2+>依赖性K^+电流（IK.Ca）和非选择性阳离子通道（IN.S），并激活IK。Ca可能是由内部储存位点的IP_3和Ca^<2+>介导的，但通过百日咳毒素不敏感的gtp结合蛋白激活in . s可能涉及不同的机制（Circulation (abstract) 1994: 90: 200）。