Intracerebroventricular (i.c.v.) infusion of the alpha1-adrenoceptor agonist phenylephrine elicits vagal and sympathetic neural stimulation of the bicarbonate secretion by the duodenal mucosa. Melatonin originating from mucosal enterochromaffin cells (EC cells) has been proposed to mediate this centrally elicited stimulation. However, the release of intestinal melatonin has not been studied. Rats were anesthetized with thiobarbiturate, a 12-mm segment of duodenum with intact blood supply was cannulated in situ and bicarbonate secretion titrated by pH-stat. The mean arterial blood pressure was continuously recorded. Melatonin in the duodenal luminal perfusate was determined by high-performance liquid chromatography with electrochemical detection. Intracerebroventricular infusion of phenylephrine (12.2 microM/kg/hr) induced more than 10-fold increase in release of melatonin into the duodenal lumen and an increase in HCO secretion from 7.6 +/- 0.5 to 18.6 +/- 2.1 microEq/cm/hr. The melatonin receptor (MT2 > MT1) antagonist luzindole (600 nM/kg, i.v.) almost abolished the marked rise in bicarbonate secretion induced by i.c.v. phenylephrine but, in contrast, did not affect the release of melatonin. These results strongly suggest that release of melatonin from the mucosa mediates the duodenal secretory response to centrally elicited neural stimulation.

中文翻译：

---

中枢神经α1肾上腺素受体刺激诱导褪黑素十二指肠腔释放。

脑室内（icv）输注α1-肾上腺素受体激动剂去氧肾上腺素引起迷走神经和十二指肠粘膜对碳酸氢盐分泌的交感神经刺激。已经提出源自粘膜肠嗜铬细胞（EC细胞）的褪黑激素介导这种中央引起的刺激。然而，尚未研究肠褪黑激素的释放。用硫代巴比妥酸盐麻醉大鼠，原位插管十二指肠段十二指肠，供血完整，并通过pH-stat滴定碳酸氢盐分泌。连续记录平均动脉血压。十二指肠腔灌注液中的褪黑素通过高效液相色谱-电化学检测法测定。脑室注射去氧肾上腺素（12。2 microM / kg / hr）导致褪黑激素释放到十二指肠腔中的释放增加了10倍以上，HCO分泌也从7.6 +/- 0.5增至18.6 +/- 2.1 microEq / cm / hr。褪黑激素受体（MT2> MT1）拮抗剂luzindole（600 nM / kg，iv）几乎消除了由icv去氧肾上腺素诱导的碳酸氢盐分泌的显着增加，但是相反，它并不影响褪黑激素的释放。这些结果强烈表明褪黑激素从粘膜的释放介导了十二指肠对中枢神经刺激的分泌反应。而去氧肾上腺素却不影响褪黑激素的释放。这些结果强烈表明褪黑激素从粘膜的释放介导了十二指肠对中枢神经刺激的分泌反应。而去氧肾上腺素却不影响褪黑激素的释放。这些结果强烈表明褪黑激素从粘膜的释放介导了十二指肠对中枢神经刺激的分泌反应。