Chariot J, Rozé C, Scarpignato C
Arch Int Pharmacodyn Ther. 1985 Mar;274(1):166-76.
The effect of the H2-receptor antagonist ranitidine on pancreatic exocrine secretion was studied in the rat. In anaesthetized animals with acute fistulas pancreatic secretion was induced by central (2-deoxy-D-glucose, 2-DG) or peripheral (acetylcholine) cholinergic stimulants and by cholecystokinin and secretin. In some experiments cimetidine was used as a reference compound. Ranitidine (20 mg X kg-1 intraperitoneally) did not change neither basal secretion nor the response to the combined hormonal stimulation. On the contrary, it significantly increased 2-DG and acetylcholine-stimulated secretion, whereas cimetidine (100 mg X kg-1 intraperitoneally) inhibited the pancreatic response to 2-DG. The different behaviour of the two H2-antagonists suggests that the effect of ranitidine is independent of the H2-receptor blockade and most probably connected with the cholinergic-like action of the drug.
在大鼠中研究了H2受体拮抗剂雷尼替丁对胰腺外分泌的影响。在具有急性瘘管的麻醉动物中，通过中枢（2-脱氧-D-葡萄糖，2-DG）或外周（乙酰胆碱）胆碱能刺激物以及胆囊收缩素和促胰液素诱导胰腺分泌。在一些实验中，西咪替丁用作参考化合物。雷尼替丁（20mg·kg-1腹腔注射）既不改变基础分泌，也不改变对联合激素刺激的反应。相反，它显著增加了2-DG和乙酰胆碱刺激的分泌，而西咪替丁（100mg·kg-1腹腔注射）抑制了胰腺对2-DG的反应。两种H2拮抗剂的不同行为表明，雷尼替丁的作用独立于H2受体阻断，很可能与该药物的类胆碱能作用有关。
