Feurle G E, Baca I, Knauf W
Regul Pept. 1982 Jul;4(2):75-82. doi: 10.1016/0167-0115(82)90097-0.
In this study the effect of 10 and 20 micrograms . kg-1 . h-1 atropine sulfate on release and pancreatic effects of neurotensin was studied in 4 dogs. Neurotensin plasma levels rose significantly when a liquid fat preparation was infused intraduodenally. This rise was almost completely abolished by simultaneous infusion of atropine. Atropine further suppressed basal and fat-stimulated output of pancreatic volume, protein, and bicarbonate; it also reduced pancreatic secretion stimulated by an intravenous infusion of low doses (2.5 to 20 pmol . kg-1 . min-1) neurotensin. The effect of higher doses (80 and 240 pmol . kg-1 . min-1 of neurotensin was less affected. As neurotensin plasma levels in contrast to normal oral feeding did not rise after sham feeding, our findings suggest that release and action of neurotensin may at least in part be dependent on a cholinergic, non-cephalic mechanism.
在本研究中，对4只犬研究了10和20微克·千克⁻¹·小时⁻¹硫酸阿托品对神经降压素释放及胰腺效应的影响。当十二指肠内输注液体脂肪制剂时，神经降压素血浆水平显著升高。同时输注阿托品几乎完全消除了这种升高。阿托品进一步抑制了胰腺体积、蛋白质和碳酸氢盐的基础分泌及脂肪刺激分泌；它还减少了静脉输注低剂量（2.5至20皮摩尔·千克⁻¹·分钟⁻¹）神经降压素所刺激的胰腺分泌。较高剂量（80和240皮摩尔·千克⁻¹·分钟⁻¹）神经降压素的效应受影响较小。由于假饲后神经降压素血浆水平与正常口服喂养相比未升高，我们的研究结果表明，神经降压素的释放和作用可能至少部分依赖于胆碱能非头端机制。
