Gronstad K, Dahlstrom A, Florence L, Zinner M J, Ahlman J, Jaffe B M
Dig Dis Sci. 1987 Apr;32(4):393-400. doi: 10.1007/BF01296293.
The mechanisms controlling vagally induced 5-HT and SP release into the jejunal lumen were studied in the cat. In control animals, electrical vagal nerve stimulation doubled the rate of endoluminal secretion of 5-HT and SP. Propranolol pretreatment did not alter luminal secretion of these hormones. Atropine suppressed motor function and induced dose-related inhibition of vagal release of endoluminal 5-HT, but not of SP; the response to hexamethonium pretreatment was similar to that of atropine. In contrast, superior cervical ganglionectomy did not alter stimulated endoluminal 5-HT release but it completely abolished release into the portal vein. The portal 5-HT release was not affected by ganglionic blockade. The data suggest that vagally mediated 5-HT release into the lumen and the portal circulation are mediated by different neural mechanisms, the former cholinergic, the latter presumably adrenergic; and release of feline 5-HT and SP are independent, suggesting two intestinal sources, the EC cell for 5-HT and peptidergic neurons for SP.
在猫身上研究了控制迷走神经诱导的5-羟色胺(5-HT)和P物质(SP)释放到空肠腔的机制。在对照动物中,迷走神经电刺激使5-HT和SP的腔内分泌速率加倍。普萘洛尔预处理未改变这些激素的腔内分泌。阿托品抑制运动功能,并诱导与剂量相关的对腔内5-HT迷走神经释放的抑制,但对SP无抑制作用;六甲铵预处理的反应与阿托品相似。相反,颈上神经节切除术未改变刺激引起的腔内5-HT释放,但完全消除了其向门静脉的释放。门静脉5-HT释放不受神经节阻断的影响。数据表明,迷走神经介导的5-HT释放到肠腔和门静脉循环是由不同的神经机制介导的,前者是胆碱能的,后者可能是肾上腺素能的;猫5-HT和SP的释放是独立的,提示有两个肠道来源,5-HT来自肠嗜铬(EC)细胞,SP来自肽能神经元。