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首页> 外文期刊>Cell and Tissue Research >beta-Adrenoceptors, but not dopamine receptors, mediate dopamine-induced ion transport in late distal colon of rats.
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beta-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多巴胺诱导的大鼠晚期结肠远端离子迁移。

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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 (alpha, beta) and dopaminergic receptors (D(1) and D(2)) were detected in the rat late distal colonic mucosa, with beta(2) displaying the highest expression. A similar result was found in human colorectal mucosa (equivalent of late distal colon in rat). Pretreatment with a beta(1)-adrenoceptor antagonist (CGP-20712A) and a beta(2)-adrenoceptor antagonist (ICI 118,551) inhibited the dopamine-induced short-circuit current response by 52.59% and 92.51%, respectively. However, neither dopamine D(1) receptor antagonist SCH-23390 nor dopamine D(2) receptor antagonist sulpiride blocked the effect of dopamine. Protein expression of both beta(1)- and beta(2)-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 beta(1)- or beta(2)-adrenoceptors. Thus, beta-adrenoceptors (mainly beta(2)-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：多巴胺是胃肠道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印迹分析以及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。在大鼠晚期远端结肠粘膜中检测到肾上腺素能受体（α，β）和多巴胺能受体（D（1）和D（2））的mRNA转录物，其中β（2）表达最高。在人结肠直肠粘膜（相当于大鼠晚期远端结肠）中也发现了类似的结果。用β（1）-肾上腺素能受体拮抗剂（CGP-20712A）和β（2）-肾上腺素能受体拮抗剂（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％。但是，无论是多巴胺D（1）受体拮抗剂SCH-23390还是多巴胺D（2）受体拮抗剂舒必利都不能阻止多巴胺的作用。在大鼠远端结肠和人类乙状结肠和直肠的粘膜中发现了β（1）-和β（2）-肾上腺素受体的蛋白表达。多巴胺显着增加转染了beta（1）-或beta（2）-肾上腺素能受体的COS-7细胞的细胞内cAMP水平。因此，β-肾上腺素能受体（主要是β（2）-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，并提供了进一步的实验证据，可能有助于预防，诊断和临床治疗人类结肠直肠疾病。

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