BACKGROUND: The aim of this study was to evaluate the effect of growth hormone releasing peptide (GHRP)-2, a synthetic ligand for the growth hormone secretagogue receptor, on upper gastrointestinal motility and food intake. METHODS: Five neurally intact dogs and five dogs with vagotomy and pyloroplasty were equipped with strain gauge force transducers on the stomach, duodenum and jejunum. GHRP-2 (0.5-10 microg/kg) was administered intravenously in neurally intact dogs in the interdigestive state and after feeding. To study the mechanism of GHRP-2-induced inhibition on postprandial contractions, various antagonists were administered intravenously prior to GHRP-2. The effect of GHRP-2 on postprandial contractions was also studied in dogs with vagotomy. GHRP-2 was also administered immediately before feeding in each group, and its effect on food intake was assessed. RESULTS: GHRP-2 did not evoke gastrointestinal contractions in the interdigestive state. GHRP-2 induced contractile inhibition continuing for 2-3 min in neurally intact dogs and dogs with vagotomy. This inhibitory effect was reversed by the alpha- and alpha(2)-blockers. GHRP-2 increased food intake in neurally intact dogs, but not in dogs with vagotomy. CONCLUSIONS: These results indicate that in the upper gut GHRP-2 inhibits postprandial contractions via alpha(2)-receptors on the enteric nervous system, whereas an intact vagal nerve is necessary for a GHRP-2-induced increase in food intake.
BACKGROUND: The aim of this study was to evaluate the effect of growth hormone releasing peptide (GHRP)-2, a synthetic ligand for the growth hormone secretagogue receptor, on upper gastrointestinal motility and food intake. METHODS: Five neurally intact dogs and five dogs with vagotomy and pyloroplasty were equipped with strain gauge force transducers on the stomach, duodenum and jejunum. GHRP-2 (0.5-10 microg/kg) was administered intravenously in neurally intact dogs in the interdigestive state and after feeding. To study the mechanism of GHRP-2-induced inhibition on postprandial contractions, various antagonists were administered intravenously prior to GHRP-2. The effect of GHRP-2 on postprandial contractions was also studied in dogs with vagotomy. GHRP-2 was also administered immediately before feeding in each group, and its effect on food intake was assessed. RESULTS:GHRP-2 did not evoke gastrointestinal contractions in the interdigestive state. GHRP-2 induced contractile inhibition continuing for 2-3 min in neurally intact dogs and dogs with vagotomy. This inhibitory effect was reversed by the alpha- and alpha(2)-blockers. GHRP-2 increased food intake in neurally intact dogs, but not in dogs with vagotomy. CONCLUSIONS: These results indicate that in the upper gut GHRP-2 inhibits postprandial contractions via alpha(2)-receptors on the enteric nervous system, whereas an intact vagal nerve is necessary for a GHRP-2-induced increase in food intake.