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A possible role as a neuromodulator of extraneuronally released-ATP.

A possible role as a neuromodulator of extraneuronally released-ATP.
可能作为神经元外释放的 ATP 的神经调节剂。
批准号:
02670102
负责人:
KATSURAGI Takeshi
金额:
$1.41万
依托单位国家:
日本
项目类别:
Grant-in-Aid for General Scientific Research (C)
财政年份:
1990
资助国家:
日本
项目状态:
已结题
起止时间:
1990 至 1991

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项目成果

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中文摘要
翻译
从1990年到1991年的研究项目试图进一步阐明豚鼠平滑肌和心肌神经外ATP释放的特征和生理作用。用荧光仪测定样品介质中ATP和乙酰胆碱的含量。n-荧光素酶测定和HPLC-ECD系统。本报告主要由以下三个内容组成。1. 平滑肌释放ATP:与p物质等其他受体激动剂相比,NA和ACh分别能有效地引起输精管和回肠的ATP释放。两种受体拮抗剂(即哌唑嗪和阿托品)均能明显抑制ATP的释放。α, β -亚甲基ATP (α, β - matp),一种p_2激动剂,也能从这些组织中产生苏拉明(p_2拮抗剂)敏感的ATP释放,表明ATP诱导-ATP释放系统的存在。在平滑肌中,递质受体刺激与肌后ATP释放之间似乎存在一种耦合机制。2. 心肌释放ATP:强心剂,如异丙肾上腺素(Iso),显著增强收缩和随后的ATP释放。丙萘洛尔可拮抗Iso对ATP释放的促进作用,而β - 2拮抗剂丁胺则不能,因此,表明释放的起源似乎主要是在点后部位。3. 神经外释放atp的作用:回肠制剂中电唤起的ach释放被α、β - matp和腺苷减少。如上所述,由于α、β - matp本身引起ATP释放,释放的ATP被酶促转化为腺苷,核苷可能调节神经传递。ATP在平滑肌中产生收缩,同时激活Ca^<2+>-内流。这两种反应都被Ca^<2+>-拮抗剂硝苯地平完全阻断,这意味着ATP激活了电压门状Ca^<2+>-通道。综上所述,通过激活平滑肌和心肌的递质受体,神经元外存在ATP释放,释放的ATP可能在自主神经传递中起到神经调节剂或神经刺激剂的作用。少
英文摘要
The research project on the above title to 1991 from 1990 was attempted to elucidate further characteristics and physiological roles of extraneurofial ATP release from smooth and cardiac muscles of guinea-pig. Amounts of ATP and ACh in sample media were measured -by a luciferi. n-luciferase assay and HPLC-ECD system, respectively. This report is mainly composed of the following three contents. 1. ATP release from smooth muscles : ATP releases from the vas deferens and ileum were effectively caused by NA and ACh, respectively, compared to other receptor agonists such as substance P. - The evo-ked-ATP release was markedly prohibited by respective receptor antagonists, i. e., prazosin and atropine. alpha, beta-Methylene ATP (alpha, beta-mATP), a P_2-agonist, also produced a suramin (P_2-antagonist) sensitive ATP release from these tissues, indicating the existence of ATP evoked-ATP release system. There seems to be a coupling mechanism between transmitters' receptor stimulation and postju … More nctional ATP release in smooth muscles. 2. ATP release from cardiac muscles : Cardiotonics, e. g., isoproterenol, (Iso), markedly enhanced the contraction and the subsequent ATP release. The enhancement by Iso of ATP release was antagonized by propranolol, but not by butoxamine, a beta_2-antagonist, thus, showing that the origin of the release seems to be, primarily, postjunctional sites. 3. Roles of extraneuronally released-ATP : Electrically evoked-ACh release from the ileal preparation was reduced by alpha, beta-mATP as well as adenosine. As stated above, since alpha, beta-mATP per se elicited the ATP release, the released ATP is enzymatically changed to adenosine and the nucleoside may modulate the neurotransmission. ATP produced a contraction coupled with activation of Ca^<2+>-influx in smooth muscles. Both the responses were completely blocked by nifedipine, a Ca^<2+>-antagonist, implying an activation by ATP of voltage gated-Ca^<2+>-channels. In conclusion, there is an extraneuronal ATP release which is elicited by activating transmitters' receptors in smooth and cardiac muscles and the released ATP may serve as a neuromodulator or a neurostimulator in autonomic neurotransmission. Less
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会议论文
桂木 猛: "シナプスへのATP動員機構ー特に非神経性組織からの遊離についてー" 日本薬理学雑誌(総説特集号). 98. 227-234 (1991)
Takeshi Katsuragi:“ATP 动员到突触的机制 - 特别是从非神经元组织中释放”日本药理学杂志(评论特刊)98. 227-234(1991)。
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共 35 条
    Identification of a specific transporter on extracellular release of ATP
    • 批准号:
      17590234
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $2.3万
    • 财政年份:
      2005
    • 负责人:
      KATSURAGI Takeshi
    • 依托单位:
    Involvement of a transporter in an autocrine / paracrine release of ATP.
    • 批准号:
      15590243
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $2.18万
    • 财政年份:
      2003
    • 负责人:
      KATSURAGI Takeshi
    • 依托单位:
    ATP-autocrine/paracrine release and its intracellular Ca^<2+> signals
    • 批准号:
      13670107
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $1.79万
    • 财政年份:
      2001
    • 负责人:
      KATSURAGI Takeshi
    • 依托单位:
    Possible involvement of CaィイD12+ィエD1-signaling transferred to mitochondria in release of ATP as an autacoid
    • 批准号:
      10670102
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $1.34万
    • 财政年份:
      1998
    • 负责人:
      KATSURAGI Takeshi
    • 依托单位:
    海外基金