Inhibition of gastric acid secretion inthe Atlantic cod, Gadus morhua, by sulphated and desulphated gastrin, caerulein, and CCK-octapeptide.
Gastric acid secretory effects of gastrin/CCK-like peptides have been assayed in cods rendered "spontaneously" secreting by a continuous intestinal perfusion with diluted (33%) seawater. A high dose of pentagastrin induced a weak stimulation (31%) of acid output, while gastrin 17-II, caerulein and CCK8 were inhibitory. Caerulein was the most potent peptide, with an estimated D50 for inhibition of 0.013 nmol/kg.h. Although displaying lower potencies, also the desulphated forms of gastrin-17, caerulein and CCK8 were inhibitory. The results may be explained by release of an endogenous inhibitor, or by interaction with endogenous "codfish gastrin". In the latter case two alternatives are considered: Either gastrin 17, CCK8, and caerulein possess lower efficacies than "codfish gastrin" and therefore act as partial agonists. Alternatively, "codfish gastrin" is itself an inhibitory principle (gastron), the effect of which is mimicked by gastrin 17, caerulein and CCK8. The actions of gastrin and the gastrin-like peptides in the cod indicate a structure-activity relationship different from previously described systems, both mammalian and submammalian.
D000818:Animals; D001067:Appetite Depressants / Q000494:pharmacology; D002108:Ceruletide / Q000494:pharmacology*; D002766:Cholecystokinin / Q000494:pharmacology*; D005260:Female; D005399:Fishes; D005744:Gastric Acid / Q000378:metabolism*; D005755:Gastrins / Q000494:pharmacology*; D008297:Male; D010446:Peptide Fragments / Q000494:pharmacology*; D012844:Sincalide
D001067:Appetite Depressants; D005755:Gastrins; D010446:Peptide Fragments; D002108:Ceruletide; D002766:Cholecystokinin; D012844:Sincalide