Animal experiment:

Rats[1]The first set of experiments is carried out on rats with intact vagus nerves which are acutely treated with CCK-8S or Gastrin-1 at the doses of 1.5, 5, 15 and 45 nmol/kg. Both these peptides are administered i.v. as a bolus immediately after the collection of basal effluent samples. In experiments investigating the involvement of muscarinic, histamine H or CCK receptors in the gastric 2 secretory responses elicited by CCK-8S or Gastrin-1, the animals are pretreated with atropine 1 μmol/kg i.v., cimetidine 10 μmolrkg i.v., devazepide 1.25-2.5 μmol/kg i.v. or L-365,260 2.5-5 μmol/kg i.v., 10 min before ending the collection of the second basal effluent sample. Additional experiments are performed in animals pretreated with the irreversible inhibitor of histidine decarboxylase, α-fluoromethylhistidine (450 mmol/kg i.p. twice daily for two consecutive days), in order to suppress endogenous histamine production from digestive enterochromaffin-like cells[1].

Gastrin-1, human is the endogenous peptide produced in the stomach, and increases gastric acid secretion via cholecystokinin 2 (CCK2) receptor.

Gastrin-1, human is the endogenous peptide produced in the stomach, and acts via cholecystokinin 2 (CCK2) receptor[1].

Gastrin-1 (1.5, 5, 15 and 45 nmol/kg, i.v.) increases pepsinogen and acid secretion in rats[1].

References:
[1]. Noble F, et al. International Union of Pharmacology. XXI. Structure, distribution, and functions of cholecystokinin receptors. Pharmacol Rev. 1999 Dec;51(4):745-81.
[2]. Blandizzi C, et al. CCK1 and CCK2 receptors regulate gastric pepsinogen secretion. Eur J Pharmacol. 1999 May 28;373(1):71-84.