Effect of duodenal osmolality on gastrin and secretin release and on gastric and pancreatic secretion.

Abstract

AbstractWe have measured the osmolality of duodenal contents in 9 dogs after a hypertonic meal, given either by mouth or directly into the stomach or perfused into the duodenum. A test meal of 2,475 mosm/kg, given by mouth, raised the intraduodenal osmolality to 700–1,500 mosm/kg over a 1‐hour period. Hypertonic glucose solutions (2,000 and 3,400 mosm/kg), given into the stomach, were found to be diluted to about 700 and 1,100 mosm/kg, respectively, at the level of the mid‐duodenum 30 minutes later. Hypertonic saline solutions (1,800 and 2,700 mosm/kg), perfused into the duodenum, created a stable intraluminal osmolality of 800 and 1,200 mosm/kg, respectively, (about 45% that of the perfusate) after 30 minutes.In 6 Heidenhain pouch dogs, gastric secretion and gastrin release stimulated by food were significantly diminished by administration of hypertonic sodium chloride solution (1,800 mosm/kg) into the duodenum. This hyperosmolality caused greater suppression of acid secretion (52%) than of gastrin release (28%). Stimulation of pancreatic water and bicarbonate secretion and of release of radioimmunoassayable secretin by intraduodenal HCl (pH 1.3) were significantly suppressed when the osmolality of the HCl solution was raised to 2,700 mosm/kg. Pancreatic protein secretion remained unchanged with hypertonic solutions. We have confirmed that stimulation of intraduodenal osmoreceptors inhibits gastric acid secretion in dogs, and we suggest that this is due, at least in part, to a suppression of gastrin release. We further suggest that duodenal osmolar inhibition of pancreatic secretion involves suppression of secretin but does not appear to involve cholecystokinin.