首页> 外文期刊>Pharmacological research: The official journal of The Italian Pharmacological Society >Lack of interaction between alpha(2)-autoreceptors and prejunctional receptors mediating a facilitatory effect on noradrenaline release.
【24h】

Lack of interaction between alpha(2)-autoreceptors and prejunctional receptors mediating a facilitatory effect on noradrenaline release.

机译:alpha(2)-autoreceptors和结前受体之间缺乏相互作用介导去甲肾上腺素释放的促进作用。

获取原文
获取原文并翻译 | 示例
获取外文期刊封面目录资料

摘要

The present study was undertaken to investigate the effect of alpha(2)-autoreceptor blockade on the facilitatory influence exerted by activation of beta -, A(2A)-adenosine- and angiotensin II receptors. Segments of a rat-tail artery, previously incubated with(3)H-noradrenaline, were subjected to electrical stimulation. The influence of isoprenaline, the compound CGS21680 and angiotensin II on the overflow of tritium evoked by electrical stimulation was checked before and after alpha(2)-adrenoceptor blockade. All the agonists used caused concentration-dependent increases of tritium overflow, the maximal effect representing increases of 44.2, 27.4 and 41.2% for isoprenaline, CGS21680 and angiotensin II, respectively. In the presence of alpha(2)-adrenoceptor blockade by phenoxybenzamine ( 1 microm) or yohimbine (33 or 100 nm), the facilitatory influence of isoprenaline, CGS21680 and angiotensin II was not significantly changed. Since this facilitatory influence, which involves the activation of G(s)- or G(q)-proteins, was not enhanced by alpha(2)-adrenoceptor blockade, it is concluded that the enhancement of the negative modulation resulting from activation of A(1)-adenosine-, muscarine- and kappa -receptors, as previously shown, should be due to the fact that the involved systems share signal transduction mechanisms, or at least G-proteins. Copyright 2000 Academic Press.
机译:进行本研究以研究α(2)-自体受体阻滞剂对激活β-,A(2A)-腺苷和血管紧张素II受体所施加的促进作用的影响。预先与(3)H-去甲肾上腺素温育的鼠尾动脉段接受电刺激。在α(2)-肾上腺素受体阻断剂之前和之后,检查异戊二烯,化合物CGS21680和血管紧张素II对电刺激诱发的the溢出的影响。所有使用的激动剂均导致concentration的浓度依赖性增加,最大作用分别代表异丙肾上腺素,CGS21680和血管紧张素II增加44.2%,27.4%和41.2%。在存在苯氧基苯甲胺(1微米)或育亨宾(33或100 nm)对α(2)-肾上腺素受体的阻断作用下,异丙肾上腺素,CGS21680和血管紧张素II的促进作用没有明显改变。由于这种促进G(s)-或G(q)-蛋白激活的促进作用并未通过alpha(2)-肾上腺素受体阻滞剂增强,因此可以得出结论,由A激活引起的负调控增强如前所示,(1)-腺苷,毒蕈碱和κ受体应归因于所涉及的系统共享信号转导机制,或至少具有G蛋白。版权所有2000学术出版社。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号