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Activation of enteric nerve pathways in the guinea‐pig duodenum by cholecystokinin octapeptide and pentagastrin.

The action and mechanism of action of cholecystokinin octapeptide (CCK‐8) and pentagastrin on isolated segments of guinea‐pig duodenum were examined using contractility studies and by intracellular recordings made from smooth muscle cells. Both CCK‐8 and pentagastrin caused an excitatory contractile response. The threshold concentration ranged from 5 X 10(‐11) to 10(‐9) M for CCK‐8 and 5 X 10(‐10) to 10(‐8) M for pentagastrin. The excitatory response was abolished by tetrodotoxin (3.1 X 10(‐6) M) and atropine (1.5 X 10(‐6) M) and inhibited by d‐tubocurarine (up to 2.9 X 10(‐5) M). In the presence of atropine a proportion of preparations relaxed in response to CCK‐8 (nineteen of thirty‐one) and pentagastrin (thirteen of seventeen). This response was only seen at high concentrations of the peptides (10(‐8)‐10(‐7) M) and was abolished by tetrodotoxin (3 X 10(‐6) M). Intracellular recordings from duodenal smooth muscle revealed multiple excitatory junction potentials (e.j.p.s) in response to CCK‐8 and to pentagastrin. These e.j.p.s were identical to those evoked by transmural nerve stimulation and were abolished by atropine (1.5 X 10(‐7) M) and by tetrodotoxin (3 X 10(‐6) M). Inhibitory junction potentials (i.j.p.s) were not recorded in response to the peptides except on one occasion. It is suggested that CCK‐8 and pentagastrin cause an increase in duodenal motility by the selective activation of excitatory pathways in the enteric nervous system.