The responses of duodenal tension receptors in sheep to pentagastrin, cholecystokinin and some other drugs.

The proposal that some post‐prandially released alimentary hormones modify ingestive behaviour and gastric emptying by altering impulse activity in alimentary enteroceptors has been tested using a number of gastrointestinal peptide hormone analogues. These and other drugs were applied to single‐unit afferent preparations of duodenal tension receptors in chloralose‐anaesthetized sheep. In separate experiments the effect of pentagastrin and cholecystokinin on duodenal motor activity was recorded without unitary afferent activity measurements. Local intra‐arterial bolus injections of pentagastrin, cholecystokinin, insulin, prostaglandin, acetylcholine, phenylbiguanide, veratrine, 5‐hydroxytryptamine and bradykinin aroused or enhanced activity in tension receptors. With the exception of a short‐latency effect of insulin B.P., these responses occurred together with local increases in tension and electromyographic activity of the duodenum. Combinations of atropine and hexamethonium reduced duodenal motor activity and abolished most drug‐evoked afferent responses. Intracarotid bolus injections of pentagastrin at first increased, then reduced duodenal tension, electromyographic activity and impulse activity of tension receptors. Cholecystokinin (CCK‐8) injected by this route caused similar alterations of these parameters, and the response was characterized by periods of reduced activity followed by a prolonged excitation of duodenal motility. From the responses to bolus injections of humoral agents it is concluded that some alimentary hormones released after a meal may have a peripheral excitatory action on the tension receptor environment which causes increased afferent activity. The mechanism probably involves both an alteration in duodenal motility and a sensitization of the receptor ending. In addition, the peptide hormones gastrin and cholecystokinin may act centrally to alter duodenal motor control and thus may influence gastric emptying and post‐prandial satiety mechanisms.