...
首页> 外文期刊>Cell and Tissue Research >β-Adrenoceptors, but not dopamine receptors, mediate dopamine-induced ion transport in late distal colon of rats
【24h】

β-Adrenoceptors, but not dopamine receptors, mediate dopamine-induced ion transport in late distal colon of rats

机译:β-肾上腺素受体而非多巴胺受体介导大鼠远端末梢结肠中多巴胺诱导的离子转运

获取原文
获取原文并翻译 | 示例
           

摘要

Dopamine, an important modulator in the gastrointestinal system, induces concentration-dependent transepithelial ion transport in the distal colon of the rat, as shown by a decrease in the short-circuit current, and acts in a segmentally dependent manner. However, the receptor(s) that mediates dopamine-induced ion transport is unknown. We have investigated the receptor mechanisms underlying dopamine-induced colonic ion transport by means of short-circuit current recording, real-time polymerase chain reaction, and Western blotting analysis, plus gene transfection and enzyme-linked immunosorbance assay. mRNA transcripts of adrenoceptors (α, β) and dopaminergic receptors (D1 and D2) were detected in the rat late distal colonic mucosa, with β2 displaying the highest expression. A similar result was found in human colorectal mucosa (equivalent of late distal colon in rat). Pretreatment with a β1-adrenoceptor antagonist (CGP-20712A) and a β2-adrenoceptor antagonist (ICI 118,551) inhibited the dopamine-induced short-circuit current response by 52.59% and 92.51%, respectively. However, neither dopamine D1 receptor antagonist SCH-23390 nor dopamine D2 receptor antagonist sulpiride blocked the effect of dopamine. Protein expression of both β1- and β2-adrenoceptors was found in the mucosa of rat distal colon and human sigmoid colon and rectum. Dopamine significantly increased intracellular cAMP levels in COS-7 cells transfected with β1- or β2-adrenoceptors. Thus, β-adrenoceptors (mainly β2-adrenoceptors), but not dopamine receptors, mediate dopamine-induced ion transport in the late distal colon of the rat. This extends our knowledge of the late distal colon (rats) or colorectum (human) and provides further experimental evidence that might aid the prevention, diagnosis, and clinical therapy of human colorectal diseases.
机译:多巴胺是胃肠系统中的重要调节剂,可引起大鼠远端结肠中浓度依赖性的跨上皮离子转运,如短路电流的减少所示,并以节段性方式起作用。但是,介导多巴胺诱导的离子转运的受体是未知的。我们已经通过短路电流记录,实时聚合酶链反应,Western印迹分析,基因转染和酶联免疫吸附测定等手段研究了多巴胺诱导的结肠离子转运的受体机制。在大鼠晚期结肠远端黏膜中检测到肾上腺素受体(α,β)和多巴胺能受体(D1 和D2 )的mRNA转录物,其中β2的表达最高。在人类结肠直肠粘膜(相当于大鼠晚期远端结肠)中也发现了类似的结果。用β1-肾上腺素受体拮抗剂(CGP-20712A)和β2-肾上腺素受体拮抗剂(ICI 118,551)预处理分别抑制多巴胺引起的短路电流响应52.59%和92.51%。然而,多巴胺D1 受体拮抗剂SCH-23390和多巴胺D2 受体拮抗剂舒必利均未阻断多巴胺的作用。在大鼠远端结肠和人乙状结肠和直肠的粘膜中发现了β1-和β2-肾上腺素受体的蛋白表达。多巴胺能明显提高转染β1-或β2-肾上腺素受体的COS-7细胞的细胞内cAMP水平。因此,β-肾上腺素能受体(主要是β2-肾上腺素能受体)而非多巴胺受体介导多巴胺诱导的大鼠晚期结肠远端离子迁移。这扩展了我们对晚期远端结肠(大鼠)或结肠直肠(人类)的认识,并提供了可能有助于预防,诊断和临床治疗人类结肠直肠疾病的进一步实验证据。

著录项

  • 来源
    《Cell and Tissue Research》 |2008年第1期|25-35|共11页
  • 作者单位

    Department of Physiology School of Basic Medical Sciences Capital Medical University Beijing 100069 People’s Republic of China;

    Department of General Surgery The First Affiliated Hospital of Zhengzhou University Zhengzhou Henan 450052 People’s Republic of China;

    Department of Chemicobiology and Pharmacy College Capital Medical University Beijing 100069 People’s Republic of China;

    Department of Physiology School of Basic Medical Sciences Capital Medical University Beijing 100069 People’s Republic of China;

    Department of Physiology School of Basic Medical Sciences Capital Medical University Beijing 100069 People’s Republic of China;

    Department of Physiology School of Basic Medical Sciences Capital Medical University Beijing 100069 People’s Republic of China;

    Department of Physiology School of Basic Medical Sciences Capital Medical University Beijing 100069 People’s Republic of China;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    Dopamine; β-Adrenoceptor; Ion transport; Late distal colon; cAMP; Rat (Sprague Dawley); Human;

    机译:多巴胺;β-肾上腺素受体;离子转运;晚期结肠末端;cAMP;大鼠(Sprague Dawley);人类;

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