SUMMARY1. Pancreatic volume flow as well as bicarbonate and protein secretion have been measured in chronic pancreatic fistula cats and dogs in response to i.v. infusion of VIP and secretin or duodenal perfusion of sodium oleate and HCl solution.2. VIP and secretin infused i.v. in cats produced superimposable pancreatic dose-response curves for volume flow and bicarbonate secretion, reaching almost identical observed and maximal calculated outputs with both peptides. In dogs, VIP was shown previously to be a much less effective stimulant of pancreatic secretion than secretin and the maximal observed bicarbonate output in response to VIP was only about 17 % of that to secretin (Konturek, Thor, Dembinski & Krol, 1975). It is concluded that VIP in cats is a secretin-like full agonist, whereas in dogs it is a partial agonist of pancreatic bicarbonate secretion.3. In cats, secretin and VIP showed equal efficacy and their combination exhibited an augmentatory action on pancreatic bicarbonate secretion with additive kinetics, whereas in dogs, VIP was found to have a lower efficacy than secretin and to inhibit competitively secretin-induced pancreatic secretion. These results might be explained by the interaction of VIP and secretin, two chemically related peptides, on a common receptor site of the exocrine pancreas.4. Caerulein, an analogue of CCK-P,, infused i.v. in cats and dogs caused a negligible pancreatic bicarbonate secretion and a potent dosedependent protein secretion. The combination of graded doses of VIP or secretin with a background dose of caerulein resulted in significantly higher bicarbonate and protein outputs than those induced by VIP or secretin alone.5. Duodenal perfusion of sodium oleate soap in cats and dogs produced pancreatic dose-response curves for volume flow and bicarbonate output similar to those evoked by VIP in these species. Pancreatic protein secretion in response to luminal oleate was slightly higher than could be S. J. KONTUREK AND OTHERS accounted for by the action of VIP alone. This might be attributed to the release by oleate not only of endogenous VIP but also CCK-P. or to the vago-vagal reflexes from gut to pancreas. The results of our combined study on cats and dogs suggest the possibility that oleate releases VIP from the gut and that this peptide may play a physiological role in the stimulation of pancreatic secretion.

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In four dogs provided with special gastroduodenal fistulas allowing for the complete separation of stomach and duodenum without interrupting the vagal connections between them, the magnitude of the gastric and intestinal phases was compared and their contribution to the total gastric response to a meal was established. A liver extract (LE) meal, confined to the stomach and maintained at pH 5.0 by an intragastric titration technique, produced acid output reaching 66% of the maximal response to histamine (MRH). Perfusion of the LE meal into the duodenum resulted in acid secretion amounting to 57% of MRH. The combination of the gastric and intestinal phases caused the highest acid output, amounting to about 90% of MRH. Gastric and intestinal phases induced separately were accompanied by a significant elevation in serum gastrin concentrations which reached the highest values when both phases were evoked simultaneously. Acidification of the intestinal meal resulted in pH-dependent inhibition of gastric secretion falling to the basal values at pH 1.0. These secretory changes were mimicked by exogenous secretin. Serum gastrin levels remained essentially unaffected by the acidification of the intestinal meal while exogenous secretin significantly lowered them. In conclusion, in the intact stomach with undisturbed nervous connections between the stomach and duodenum, a peptone meal in the intestine is capable of evoking a potent gastric acid and pepsin stimulation by a mechanism involving the release of antral hormone.

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SUMMARY1. The gastric and intestinal phases of gastric secretions were selectively evoked before and after the removal of the antral mucosa in four dogs provided with a special cannula that allowed complete separation of the stomach and duodenum without interrupting neural connexions between them.2. The gastric phase induced by 5 % liver extract meal administered into the stomach at various distention pressures (ranging from 0 to 15cm H20) resulted in an increase in acid output to about 56 % of the histamine maximum and in a marked rise in serum gastrin.3. Following resection of the antral mucosa, the gastric acid response to meal of liver extract was reduced by about 50 % and serum gastrin response was completely eliminated. Exogenous gastrin (G-17) given during the gastric phase induced by such a meal in dogs with antral mucosectomy failed to restore acid output to pre-resection level. 4. Intestinal perfusion of meal of liver extract in graded amounts stimulated gastric acid secretion to about 30 % of histamine maximum acid output and raised significantly serum gastrin level. 5. Antral mucosectomy abolished almost completely both gastric acid and serum gastrin response to intestinal meal of liver extract.6. Exogenous gastrin given during the intestinal meal of liver extract failed to restore acid output to the pre-resection level, suggesting that this procedure greatly reduced the secretary capacity of the oxyntic glands.7. We conclude that the antral gland area plays an important role in the gastric phase and that it is a prerequisite for the intestinal phase of gastric secretion.