改变prejunctional调制alpha2-adrenoceptors肠道胆碱能和去甲通路的实验性结肠炎的存在。

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Blandizzi C, Fornai M,科鲁奇R, Baschiera F,芭芭拉·G·德·乔治·R·德·庞帝F, Breschi MC,德尔Tacca M

改变prejunctional调制alpha2-adrenoceptors肠道胆碱能和去甲通路的实验性结肠炎的存在。

Br杂志。2003;139 (2):309 - 20。

PubMed ID

12770936 (在PubMed

]

文摘

1本研究调查的影响肠道炎症:(1)肠道神经传递的控制和运动性prejunctionalα(2)-adrenoceptors和(2)肠道α(2)-adrenoceptors的表达。引起的实验性结肠炎是intrarectal管理2,4-dinitrobenzenesulphonic酸(dnb)老鼠。英国2 - 14304抑制atropine-sensitive回肠和结肠纵肌电诱发收缩准备。英国- 14304具有类似行动效力,但更高的功效,在组织DNBS-treated动物;其影响的敌意比rauwolscine通过酚妥拉明与更大的力量。3电诱导((3)H)去甲肾上腺素释放回肠准备在结肠炎的存在降低了。氚流出减少了英国- 14304和刺激了rauwolscine或酚妥拉明:这些影响是增强与结肠炎准备从动物。4逆转录-聚合酶链反应和免疫印迹试验证明了蛋白表达α(2)-adrenoceptors从回肠和结肠粘膜和肌肉组织隔离。结肠炎的感应增加α(2)肾上腺素受体表达在回肠和结肠肌层,未伴有粘膜组织的变化。5感应结肠炎木炭悬架体内的胃肠推进。 In this setting, the gastrointestinal transit was inhibited by intraperitoneal (i.p.) UK-14,304 and stimulated by i.p. rauwolscine. After pretreatment with guanethidine, the stimulant action of rauwolscine no longer occurred, and UK-14,304 exerted a more prominent inhibitory effect that was antagonized by rauwolscine. 6 The present results indicate that, in the presence of intestinal inflammation, prejunctional alpha(2)-adrenoceptors contribute to an enhanced inhibitory control of cholinergic and noradrenergic transmission both at inflamed and noninflamed distant sites. Evidence was obtained that such modulatory actions depend on an increased expression of alpha(2A)-adrenoceptors within the enteric nervous system.

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药物靶点

药物	目标	类	生物	药理作用	行动
酚妥拉明	Alpha-2A肾上腺素能受体	蛋白质	人类	是的	拮抗剂	细节