gastrins and Hyperemia

1. Cholecystokinin octapeptide (CCK-8) and gastrin-17 augment gastric mucosal blood flow in the rat. The present study examined whether the gastric vasodilator effect of these peptides is mediated by CCKA or CCKB receptors. 2. Intravenous injection of CAM-1481 (1 mg kg-1), a dipeptoid antagonist of CCKA receptors, or CAM-1028, a dipeptoid CCKB receptor antagonist (1 mg kg-1), had no effect on basal gastric mucosal blood flow as determined by the clearance of hydrogen in urethane-anaesthetized rats. 3. Intravenous infusion of CCK-8 or gastrin-17 (8-200 pmol min-1) increased gastric mucosal blood flow in a dose-dependent fashion. The CCKB receptor antagonist, CAM-1028, significantly attenuated the hyperaemic response to CCK-8 and gastrin-17 whereas the CCKA receptor antagonist, CAM-1481, did not antagonize CCK-8 but caused a slight attenuation of the vasodilator response to gastrin-17. 4. The selectivity of the two antagonists was proved by the findings that CAM-1028, but not CAM-1481, inhibited gastric acid secretion evoked by CCK-8 or gastrin-17 (CCKB receptor assay) while CAM-1481, but not CAM-1028, inhibited the CCK-8-induced contraction of guinea-pig isolated gall bladder strips (CCKA receptor assay). 5. These data show that the actions of CCK-8 and gastrin-17 to increase mucosal blood flow in the rat stomach are primarily mediated by CCKB receptors.

Topics: Animals; Cholecystokinin; Dipeptides; Female; Gallbladder; Gastric Acidity Determination; Gastric Mucosa; Gastrins; Guinea Pigs; Hyperemia; In Vitro Techniques; Indoles; Meglumine; Muscle Contraction; Muscle, Smooth; Rats; Rats, Sprague-Dawley; Receptors, Cholecystokinin; Regional Blood Flow; Vasodilation

The gastric mucosa of 19 mongrel dogs was submitted to a bilio-pancreatic, isolated biliary or isolated pancreatic reflux. With an isolated biliary reflux, there is a more rapid and more severe hyperaemia and foveolar hyperplasia of the mucosa of the fundus than with an isolated pancreatic reflux. There was no significant change in the basal serum level of gastrin with any of these different types of alkaline reflux, but we observed a statistically significant increase in the level of histamine in the gastric mucosa. Hyperaemia and foveolar hyperplasia of the fundic mucosa both disappeared when the alkaline reflux was suppressed, and there was a statistically significant decrease in the basal serum level of gastrin and in the level of histamine in the gastric mucosa.

Topics: Animals; Bile Reflux; Biliary Tract Diseases; Dogs; Duodenogastric Reflux; Gastric Mucosa; Gastrins; Gastritis; Gastrostomy; Histamine; Hyperemia; Jejunum; Time Factors

Topics: Animals; Coloring Agents; Dogs; Electric Stimulation; Gastric Mucosa; Gastrins; Gastrointestinal Motility; Hydrogen-Ion Concentration; Hyperemia; Stomach; Vagotomy; Vagus Nerve