CCK and gastrin inhibit adenylate cyclase activity through a pertussis toxin-sensitive mechanism in the tumoral rat pancreatic acinar cell line AR 4-2J (original) (raw)

Thr28,Nleat)CCK(23-33) (CCK-9) and gastrin(1-17)l (gastrin) inhibited adenylate cyclase activity in membranes from the tumoral rat pancreatic acinar cell line AR 4-2J through a Bordetella pertussis toxin-sensitive mechanism. This contrasted with the stimulatory effect exerted by CCK-9 on adenylate cyclase activity in membranes from normal rat pancreas. The relative potency of CCK-9, gastrin, and related peptides in inhibiting adenylate cyclase, when confronted with previous evidence, suggests that 'non-selective CCK-gastrin CCK-B receptors' predominating over 'selective CCK-A receptors' in the AR 4-2J cell line, favored the coupling of the first receptors to adenylate cyclase through G, while CCK-A receptors capable of stimulating the enzyme through Gs were detected only after Bordetella pertussis toxin pretreatment. Cholecystokinin receptor; Gastrin receptor; Adenylate cyclase; Guanine nucleotide-binding regulatory protein; Pertussis toxin; (Rat pacreas, Tumoral rat pancreatic cell line AR 4-2J) Published by Elsevier Science Publishers B.V. (Biomedical Division) 00145793/88/$3.50