Antidromic nerve regulation and effecter protection by ATP released from effector cell
Antidromic nerve regulation and effecter protection by ATP released from effector cell
批准号:
14570094
负责人:
SHINZOUKA Kazumasa
金额:
$2.11万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2002
资助国家:
日本
项目状态:
已结题
起止时间:
2002 至 2003
中文摘要
研究了三磷酸腺苷对神经递质逆向调节的保护作用。(1)三磷酸腺苷释放机制的分布:在11种组织制剂中,10赫兹的电刺激(ES)可引起三磷酸腺苷的释放。(2)神经刺激引起的ATP释放,ES对去甲肾上腺素(NA)和嘌呤类化合物的释放呈频率依赖性增加。此外,嘌呤类化合物的释放量随NA浓度的增加而增加。因此,我们认为嘌呤化合物的释放依赖于神经系统的兴奋。(3)释放三磷酸腺苷的保护作用:抑制NA的释放:在高频下,三磷酸腺苷和α-受体激动剂在较高浓度时产生嘌呤化合物的释放,内源性嘌呤抑制交感神经中的去甲肾上腺素的释放。(4)释放三磷酸腺苷的保护作用:促进通透性:我们观察到…用培养的大鼠尾动脉内皮细胞进行的实验表明,嘌呤能受体激动剂能促进血管内皮细胞层的通透性。(5)与疾病的关系:生活方式相关疾病大鼠的逆向调节功能障碍。交感神经末梢上的嘌呤能受体在遗传性生活方式相关疾病大鼠(SHR/NDmcrcp)中不起作用。这些结果提示:当动脉交感神经极度兴奋时,内源性嘌呤被释放,抑制神经传递,从而改善血流,进而增加内皮细胞的通透性,改善对周围组织的物质运输。因此,ATP似乎通过这两条途径保护周围效应组织,并可能是生活方式相关疾病发生和发展的重要因素。较少
英文摘要
The protective role of antidromic regulation of neurptransmission by ATP was examined.(1)The distribution of mechanism of ATP release :In the 11 kinds of tissue preparations, electrical stimulation(ES) at 10Hz elicited the release of ATP. In the caudal artery, the amount of ATP-release was the most.(2)ATP release by nerve stimulation.The releases of noradrenaline(NA) and purine compounds by ES were increased in frequency-dependent manner. In addition, the release of purine compounds was increased in the NA concentration dependent manner. Therefore, it was suggested that release of a purine compounds depends on the excitation of the nervous system.(3)Protective effect by release ATP : Inhibitory action on NA-release :ES at high frequency, ATP and alpha-adrenoceptor agonist at higher concentration produced release of purine compound, and the endogenous purines inhibit the release of NA from sympathetic nerves.(4)Protective effect by release ATP : promotion of permeability :We observed th … More at the permeability of the vascular endothelium cell layer was promoted by purinergic receptor agonist, by the experiment using culture endothelial cells of rat caudal artery. This permeable promotion was also observed in rat caudal artery preparation.(5)Relation with disease : Dysfunction of antidromic regulation in life-style-related diseases of rat.Purinergic receptor on the sympathetic nerve ending did not function in genetic life-style related diseases rat(SHR/NDmcrcp). The release of endogenous purines was not changed in the disease model rat.These results suggested the following hypothesis ; When the arterial sympathetic nerve was excited extremely, an endogenous purines were released and inhibited neurotransmission and then improved bloodstream, and furthermore enhanced in permeability of endothelial cell layer and improved material transport to peripheral tissues. So, ATP seems to protect peripheral effector tissues through these two pathways, and may be important factor on the onset and development of life-style related diseases. Less
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Shinozuka K. et al.: "Purinergic modulation of vascular symoathetic neurotransmission."Jananese Journal of Pharmacology. 88. 19-25 (2002)
Shinozuka K.等人:“血管交感神经传递的嘌呤能调节。”Jananese Journal of Pharmacology。
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橋本道男, 田中直子, 藤井由已, 窪田洋子, 篠塚和正, 国友 勝、紫藤 治: "ニコランジルによる血管内皮細胞からのATP遊離促準作用にミトコンドリアATP感受性K^+チャネルは関与するか?"Therapeutic Research. 24. 0-15 (2003)
Michio Hashimoto、Naoko Tanaka、Yoshimi Fujii、Yoko Kubota、Kazumasa Shinozuka、Masaru Kunitomo、Osamu Shito:“线粒体 ATP 敏感 K^+ 通道是否参与尼可地尔促进血管内皮细胞释放 ATP?” 24 0-15 (2003)
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Shinozuka K. et al.: "Purinergic modulation of vascular sympathetic neurotransmission."Japanese Journal of Pharmacology. 88. 19-25 (2002)
Shinozuka K.等人:“血管交感神经传递的嘌呤能调节。”日本药理学杂志。
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Tanaka N. et al.: "P2Y-receptor regulates size of endothelial cells in an intracellular Ca(2+) dependent manner"Life Science. 72. 1445-1453 (2003)
Tanaka N. 等人:“P2Y 受体以细胞内 Ca(2) 依赖性方式调节内皮细胞的大小”生命科学。
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Tanaka N. et al.: "P2Y receptor-mediated enhancement of permeation requires Ca^<2+> signalling in vascular endothelial cells"Clinical and Experimental Pharmacology and Physiology. 30. 649-652 (2003)
Tanaka N.等人:“P2Y受体介导的渗透增强需要血管内皮细胞中的Ca 2+ 信号传导”临床和实验药理学和生理学。
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