Gastrin I£¬Human£¬IC-0321080

The peptide cholecystokinin (CCK), originally discovered in the gastrointestinal tract, has been shown to mediate pancreatic secretion and contraction of gallbladder. Two types of CCK receptors (CCK₁ found in the gut and CCK₂ found in the brain) have thus been distinguished. Gastrin-1, human, a endogenous peptide produced in the stomach, increases gastric acid secretion via acting at CCK₂ receptor^[1]. In anaesthetized rats, gastrin-1, human (1.5, 5, 15 and 45 nmol/kg, i.v.) increased both pepsinogen and acid secretion. After pretreatment with omeprazole, gastrin-1, human failed to stimulate acid secretion, while it increased pepsinogen output. In rats with gastric perfusion of acid solutions, gastrin-1, human increased peptic output in a pH-independent manner either with or without pretreatment with omeprazole^[2].

¡¾1¡¿Noble F, et al. International Union of Pharmacology. XXI. Structure, distribution, and functions of cholecystokinin receptors. Pharmacol Rev. 1999 Dec;51(4):745-81

¡¾2¡¿Blandizzi C, et al. CCK1 and CCK2 receptors regulate gastric pepsinogen secretion. Eur J Pharmacol. 1999 May 28;373(1):71-84