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

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Abstract
(Thr28,Nle31)CCK(23-33) (CCK-9) and gastrin(1-17)1 (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(i), while CCK-A receptors capable of stimulating the enzyme through G(s) were detected only after Bordetella pertussis toxin pretreatment.SCOPUS: ar.jinfo:eu-repo/semantics/publishe