Lu Q H, Greeley G H, Zhu X G, Thompson J C
Endocrinology. 1984 Jun;114(6):2415-7. doi: 10.1210/endo-114-6-2415.
The effect of intracerebroventricular (ICV) administration of cholecystokinin-8 (CCK-8) (0.5, 1.0, 2.0, 4.0 micrograms) on plasma levels of pancreatic polypeptide (PP) was studied in conscious dogs. ICV administration of CCK-8 (1.0, 2.0, 4.0 micrograms) produced a rapid and transient elevation in plasma concentrations of PP. Peripheral muscarinic receptor blockade with atropine or truncal vagotomy abolished PP secretion induced by ICV CCK-8. Pretreatment with ICV atropine also prevented the elevation in plasma PP induced by CCK-8. Plasma levels of CCK-33/39, CCK-8, and gastrin were not affected by ICV CCK-8. Our results indicate that central administration of CCK-8 selectively elevated plasma PP concentration. Since the effect of CCK-8 on plasma PP was abolished by central and peripheral atropine pretreatment, as well as by vagotomy, central and peripheral vagal cholinergic mechanisms appear to participate in release of PP that is induced by CCK-8 given by ICV injection.
在清醒的犬中研究了脑室内(ICV)注射胆囊收缩素-8(CCK-8)(0.5、1.0、2.0、4.0微克)对胰多肽(PP)血浆水平的影响。ICV注射CCK-8(1.0、2.0、4.0微克)导致PP血浆浓度迅速且短暂升高。用阿托品进行外周毒蕈碱受体阻断或切断迷走神经干可消除ICV CCK-8诱导的PP分泌。ICV阿托品预处理也可防止CCK-8诱导的血浆PP升高。ICV CCK-8对CCK-33/39、CCK-8和胃泌素的血浆水平无影响。我们的结果表明,中枢给予CCK-8可选择性升高血浆PP浓度。由于CCK-8对血浆PP的作用可被中枢和外周阿托品预处理以及迷走神经切断所消除,因此中枢和外周迷走胆碱能机制似乎参与了ICV注射CCK-8诱导的PP释放。