Inhibitory effect of somatostatin on cholecystokinin release is independent of luminal cholecystokinin-releasing factor content in conscious rats

Introduction: Exclusion of bile-pancreatic juice from the intestine increas es pancreatic secretion via cholecystokinin (CCK) release in conscious rats . Luminal CCK-releasing factor (LCRF), purified from rat intestinal secreti ons. is an intraluminal regulator of CCK secretion during bile-pancreatic j uice diversion. Aims: Because somatostatin is a potent inhibitor of CCK release and pancrea tic secretion, the inhibitory effect of somatostatin on LCRF was examined. Methodology: Rats were prepared with bile and pancreatic cannulae and two d uodenal cannulae and with an external jugular vein cannula. The experiments were conducted without anesthesia. After 1.5-hour basal collection of panc reatic juice with bile-pancreatic juice return, bile-pancreatic juice was d iverted for 2 hours, during which time somatostatin (2, 10 nmol/kg/h) was i nfused intravenously. The rats were killed before and 1 and 2 hours after b ile-pancreatic juice diversion. To examine the effect of luminal somatostat in, 50 or 200 nmol/kg/h of somatostatin was infused into the duodenum. The plasma CCK and luminal content of LCRF were measured by specific radioimmun oassays. Results: Bile-pancreatic juice diversion significantly increased pancreatic secretion. plasma CCK, and LCRF levels. Intravenous infusion of somatostat in inhibited CCK release and pancreatic secretion, but not LCRF content. Lu minal administration of somatostatin did not show any effect. Conclusion: Inhibitory effect of circulating somatostatin on CCK release an d pancreatic secretion is independent of LCRF content.