Pascaud X B, Chovet M, Roze C, Junien J L
Institut de Recherche Jouveinal, Fresnes, France.
Eur J Pharmacol. 1993 Feb 16;231(3):389-94. doi: 10.1016/0014-2999(93)90115-x.
Neuropeptide Y (NPY) has been shown to mimic the effects of some sigma receptor agonists in the brain and to possess the same proabsorptive effect as these agonists in the isolated mouse jejunum. The aim of present study was to investigate the effect of NPY on duodenal alkaline secretion in the rat and to define its mode of action. NPY (0.01 to 3 micrograms/kg i.v.) induced a dose-related increase in duodenal bicarbonate secretion, the maximal effect being obtained at 1 micrograms/kg. This response was significantly inhibited by the i.v. administration of haloperidol, BMY 14802, devazepide, hexamethonium, tetrodotoxin and by bilateral truncal vagotomy, but not by SCH 23390, sulpiride, prazosin or atropine, whereas i.c.v. devazepide had no effect. This pharmacological profile is identical to that reported for sigma receptor agonists. The results suggest that NPY and sigma ligands act through a common pathway to stimulate duodenal alkaline secretion in the rat.
神经肽Y(NPY)已被证明可模拟某些σ受体激动剂在大脑中的作用,并在离体小鼠空肠中具有与这些激动剂相同的促吸收作用。本研究的目的是研究NPY对大鼠十二指肠碱性分泌的影响,并确定其作用方式。静脉注射NPY(0.01至3微克/千克)可引起十二指肠碳酸氢盐分泌呈剂量相关增加,在1微克/千克时达到最大效应。静脉注射氟哌啶醇、BMY 14802、地伐西匹、六甲铵、河豚毒素以及双侧迷走神经干切断术可显著抑制该反应,但SCH 23390、舒必利、哌唑嗪或阿托品则无此作用,而脑室内注射地伐西匹则无效。这种药理学特征与报道的σ受体激动剂相同。结果表明,NPY和σ配体通过共同途径刺激大鼠十二指肠碱性分泌。