MUCOSAL MAST-CELLS ARE INVOLVED IN CCK DISRUPTION OF MMC IN THE RAT INTESTINE

Our aim was to determine if mucosal mast cells could be activated by e ndogenous CCK and, as a consequence, mediate CCK actions in the small intestine. Rats were prepared for electromyography to record electrica l activity in the small intestine. In another group of animals, the du odenum was perfused to measure rat mast cell protease II (RMCP II) as indicative of mast cell degranulation. Endogenous CCK release was indu ced by administration of soybean trypsin inhibitor (SBTI) in conscious rats or by intraduodenal perfusion of ovalbumin hydrolysate (OVH) in anesthetized rats. CCK concentration was measured by bioassay on pancr eatic acini. SBTI in control rats disrupted migrating motor complexes (MMC) for >40 min. In rats treated with the mast cell stabilizer ketot ifen, SBTI did not induce any change in the MMC pattern. RMCP II conce ntration in the duodenal perfusate significantly increased after OVH. Perfusate from ketotifen-treated animals did not show any significant increase in RMCP II values during OVH perfusion, although CCK plasma c oncentration was not different from the control group. Furthermore, in fusion of the CCK-B receptor antagonist L-365,260 significantly blocke d the increase of RMCP II concentration after OVH. Our results indicat e that mucosal mast cells are degranulated by endogenous CCK release t hrough stimulation of CCK-B receptors. Therefore mucosal mast cells pa rticipate in CCK intestinal actions.