Evidence that cholecystokinin octapeptide (CCK-8) acts as a potent, full agonist on gastrin receptors for acid secretion in the isolated mouse stomach: lack of antagonism by the specific CCK antagonist asperlicin.
Cholecystokinin octapeptide (CCK-8) (EC50 = 5 nM) was considerably more potent than pentagastrin (EC50 = 161 nM) in stimulating acid secretion in the isolated perfused mouse stomach suspended in a medium containing a phosphodiesterase inhibitor. The maximum acid response to CCK-8 was not significantly different from that produced by pentagastrin. The nonselective CCK/gastrin antagonist, proglumide, but not the selective CCK antagonist, asperlicin, antagonized the acid response to both pentagastrin and CCK-8. The data suggest that CCK-8 acts as a potent, full agonist on gastrin receptors for acid secretion in the isolated mouse stomach.
D000818:Animals; D001570:Benzodiazepinones / Q000494:pharmacology*; D005260:Female; D005744:Gastric Acid / Q000378:metabolism; D005753:Gastric Mucosa / Q000187:drug effects* / Q000378:metabolism; D066298:In Vitro Techniques; D051379:Mice; D010418:Pentagastrin / Q000494:pharmacology; D011949:Receptors, Cholecystokinin / Q000187:drug effects* / Q000502:physiology; D012844:Sincalide / Q000494:pharmacology*
D001570:Benzodiazepinones; D011949:Receptors, Cholecystokinin; D010418:Pentagastrin; D012844:Sincalide; C046367:asperlicin