Makovec F, Bani M, Cereda R, Chistè R, Pacini M A, Revel L, Rovati L C
Pharmacol Res Commun. 1987 Jan;19(1):41-51. doi: 10.1016/0031-6989(87)90031-2.
Cholecystokinin (CCK) is a hormonal regulator of the motility of the gallbladder. CCK-8, i.e. the biologically active C-terminal octapeptide of the hormone, elicits contraction and emptying of the gallbladder. Endogenous CCK released by egg yolk or fatty acids in the duodenum gives the same results. CR 1409 (lorglumide), a glutaramic acid derivative with peripheric competitive CCK-antagonistic activity, was evaluated in comparison with proglumide (the model CCK-receptor antagonist) and other conventional antispasmodic drugs, for their ability to inhibit the emptying of the gallbladder induced in mice by CCK-8 or by lyophylized egg yolk. CR 1409 (1-10 mg/kg) prevented dose-dependently the emptying of the gallbladder in both experimental models; proglumide exhibited a comparable activity at much higher doses (200-800 mg/kg). On the contrary the anticholinergic drug atropine, the calcium-antagonist nifedipine, and the phosphodiesterase inhibitor papaverine were almost ineffective. The present data support the hypothesis that the effects of CCK on gallbladder motility are mediated by a CCK-dependent specific mechanism.
胆囊收缩素（CCK）是胆囊运动的一种激素调节因子。CCK-8，即该激素具有生物活性的C末端八肽，可引起胆囊收缩和排空。十二指肠中由蛋黄或脂肪酸释放的内源性CCK也会产生相同的结果。与丙谷胺（典型的CCK受体拮抗剂）和其他传统解痉药物相比，对具有外周竞争性CCK拮抗活性的谷氨酸衍生物CR 1409（洛谷胺）抑制CCK-8或冻干蛋黄诱导的小鼠胆囊排空的能力进行了评估。CR 1409（1 - 10毫克/千克）在两种实验模型中均剂量依赖性地阻止了胆囊排空；丙谷胺在高得多的剂量（200 - 800毫克/千克）时表现出类似活性。相反，抗胆碱能药物阿托品、钙拮抗剂硝苯地平和磷酸二酯酶抑制剂罂粟碱几乎无效。目前的数据支持这样的假说，即CCK对胆囊运动的作用是由一种依赖CCK的特定机制介导的。
