Chang R S, Lotti V J, Chen T B
Life Sci. 1985 Mar 11;36(10):965-71. doi: 10.1016/0024-3205(85)90392-3.
CCK-octapeptide (CCK-8) (EC50 = 0.5 nM), in the presence of Li+, increased 3H-inositol phosphate (IP) accumulation in guinea pig gastric glands prelabeled with 3H-inositol. CCK-8 desulfate, human gastrin I and pentagastrin were much less potent than CCK-8. Antagonists of CCK receptors such as proglumide, dibutyryl-c-GMP and CBZ-Tyr (SO3H)-Met-Gly-Trp-Met-AspNH2 shifted the CCK dose response curve to the right. However, histamine (H1 and H2), cholinergic, substance P and alpha- and beta-adrenergic receptor antagonists had no effect on 3H-IP accumulation induced by CCK. The results suggest that CCK receptor activation in gastric glands leads to an enhanced breakdown of inositol phospholipids which may relate to calcium mobilization and pepsinogen secretion.
在锂离子存在的情况下，胆囊收缩素八肽（CCK-8）（EC50 = 0.5纳摩尔）可增加预先用3H-肌醇标记的豚鼠胃腺中3H-肌醇磷酸（IP）的积累。CCK-8去硫酸盐、人胃泌素I和五肽胃泌素的效力远低于CCK-8。CCK受体拮抗剂如丙谷胺、二丁酰环鸟苷酸和CBZ-酪氨酸（磺酸）-甲硫氨酸-甘氨酸-色氨酸-甲硫氨酸-天冬酰胺将CCK剂量反应曲线右移。然而，组胺（H1和H2）、胆碱能、P物质以及α和β肾上腺素能受体拮抗剂对CCK诱导的3H-IP积累没有影响。结果表明，胃腺中CCK受体的激活导致肌醇磷脂分解增强，这可能与钙动员和胃蛋白酶原分泌有关。
