Ando M, Kim H T, Takase I, Kawahara A
Zoolog Sci. 2000 Apr 1;17(3):307-12. doi: 10.2108/jsz.17.307.
Guanabenz, an I2-imidazoline-related compound with high affinity for intestinal membrane of the eel (), enhanced the transepithelial potential difference (PD) and short-circuit current (Isc) from serosa to mucosa after pretreatment with isobutylmethylxanthine (IBMX), serotonin (5-HT) and methacholine (MCh). The mucosal effect of guanabenz was not mimicked by adrenaline, indicating that the mucosal guanabenz binding site is not adrenoceptors. The mucosal guanabenz enhanced the Isc in a concentration-dependent manner. Similar enhancement in the Isc was also obtained after addition of other imidazoline derivatives such as ST93, clonidine, ST91, naphazoline and UK14,304 into the mucosal fluid. On the other hand, the effect of guanabenz was completely blocked by mucosal RX821002 or efaroxan, another imidazoline derivatives. Since some imidazoline derivatives act as agonists and others as antagonist, there must exist imidazoline receptor on the mucosal side of the eel intestine. Accompanied by an increase in the PD, NaCl and water absorption across the intestine was also enhanced by mucosal guanabenz. To search for endogenous ligands for the imidazoline receptor, luminal fluid in the intestine of the seawater eels was collected. However, most luminal fluid was ineffective. Only one among 10 samples showed guanabenz-like activity, suggesting that the endogenous ligands is secreted into the lumen under restricted condition alone.
胍那苄是一种与咪唑啉相关的化合物，对鳗鱼肠膜具有高亲和力，在用异丁基甲基黄嘌呤（IBMX）、5-羟色胺（5-HT）和乙酰甲胆碱（MCh）预处理后，可增强从浆膜到黏膜的跨上皮电位差（PD）和短路电流（Isc）。肾上腺素不能模拟胍那苄的黏膜效应，这表明黏膜胍那苄结合位点不是肾上腺素能受体。黏膜胍那苄以浓度依赖的方式增强Isc。向黏膜液中添加其他咪唑啉衍生物如ST93、可乐定、ST91、萘甲唑啉和UK14,304后，也获得了类似的Isc增强效果。另一方面，胍那苄的效应被黏膜RX821002或另一种咪唑啉衍生物依酚氯铵完全阻断。由于一些咪唑啉衍生物起激动剂作用，而另一些起拮抗剂作用，鳗鱼肠道黏膜侧必定存在咪唑啉受体。伴随PD的增加，黏膜胍那苄还增强了NaCl和水在肠道的吸收。为了寻找咪唑啉受体的内源性配体，收集了海水鳗鱼肠道的肠腔液。然而，大多数肠腔液没有效果。10个样本中只有1个显示出胍那苄样活性，这表明内源性配体仅在受限条件下分泌到肠腔中。
