Effect of duodenal juice on bombesin‐stimulated cholecystokinin release during loxigIumide administration in man

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Abstract
Stimulation of cholecystokinin release by bombesin is augmented by cholecystokinin receptor blockade with loxiglumide. We hypothesize that this augmented cholecystokinin release results from inhibition of the pancreatico‐biliary response to bombesin during cholecystokinin receptor blockade. To test this hypothesis, we infused bombesin for 180 min in six healthy subjects Three bombesin‐infusion experiments were performed in each subject in random order on different days. In two of these experiments loxiglumide was co‐infused with bombesin, while in the third experiment saline was co‐infused with bombesin. In one of the loxiglumide experiments, duodenal juice, collected on the previous day during infusion of cholecystokinin‐GIH, was reperfused intraduodenally during the second hour of bombesin infusion.In the saline experiment, the integrated cholecystokinin response during the first hour of bombesin‐infusion (262 ± 63 pmol 60 min‐1) was significantly (P < 0.01) higher than during the second (88 ± 26 pmol 60 min‐1) and third (87 ± 31 pmol 60 min‐l) hour of bombesin‐infusion. Loxiglumide augmented bombesin‐stimulated cholecystokinin secretion from 262 ± 63 pmol 60 min‐1 to 453 ± 63 pmol 60 min‐1 in the first hour of bombesin infusion (P < O.01). Integrated cholecystokinin values in the second (489 ± 90 pmol 60 min‐1) and third (450 ± 74 pmol 60 min‐1) hour of the loxiglumide experiment, were significantly (P < 0.01) higher than in the saline experiment. Duodenal juice significantly (P‐1 in the first hour of reperfusion, and from 450 ± 74 to 300 ±85 pmol 60 min‐1 in the hour after reperfusion (P<0.05). However, during and after reperfusion of duodenal juice, cholecystokinin concentrations were still distinctly (P<0.01) higher than in the BBS without loxiglumide experiment.Since the presence of bombesin‐like immunoreac‐tivity in the mucosa of the small intestine permits a role for this neuropeptide in the regulation of cholecystokinin release under physiological conditions, and since the present study demonstrates that pancreatico‐biliary outputs suppress the augmented cholecystokinin response to bombesin during specific blockade of CCK‐receptors, this study supports the concept that pancreatico‐biliary components in the duodenum may be involved in a feedback regulation between pancreatico‐biliary products and cholecystokinin release in man.