Schepp W, Ruoff H J, Maśliński S
Arch Int Pharmacodyn Ther. 1983 Oct;265(2):293-308.
The inhibitory properties of secretin, vasoactive intestinal polypeptide (VIP), cholecystokinin (CCK), somatostatin and prostaglandin E2 (PGE2) on acid production in response to histamine were tested in vitro by measuring the 14C-aminopyrine (14C-AP) uptake into isolated rat parietal cells, a reliable index of H+ generation. All compounds significantly inhibited 14C-AP accumulation and 4 X 10(-8) mol/l secretin, 7 X 10(-8) mol/l PGE2 and 2 X 10(-7) mol/l CCK decreased the effect of 10(-4) mol/l histamine by 50% (IC50). VIP and somatostatin did not reduce AP-uptake to such extent and the approximate IC50 values could not be established. The type of inhibition by all peptides and PGE2 appeared not to be competitive in nature. Our data suggest that these compounds inhibit acid production by a mechanism localized directly at the parietal cell and that secretin and CCK are unlikely to exert a physiological role as inhibitors of gastric acid secretion.
通过测量14C-氨基比林(14C-AP)进入分离的大鼠壁细胞的摄取量(这是H+生成的可靠指标),在体外测试了促胰液素、血管活性肠肽(VIP)、胆囊收缩素(CCK)、生长抑素和前列腺素E2(PGE2)对组胺刺激的胃酸分泌的抑制特性。所有化合物均显著抑制14C-AP的积累,4×10(-8)mol/L促胰液素、7×10(-8)mol/L PGE2和2×10(-7)mol/L CCK可使10(-4)mol/L组胺的作用降低50%(半数抑制浓度)。VIP和生长抑素并未将AP摄取量降低到如此程度,因此无法确定其大致的半数抑制浓度值。所有肽类和PGE2的抑制类型似乎并非竞争性抑制。我们的数据表明,这些化合物通过直接作用于壁细胞的机制来抑制胃酸分泌,并且促胰液素和CCK不太可能作为胃酸分泌抑制剂发挥生理作用。