MEDIATION BY CCKB RECEPTORS OF THE CCK-EVOKED HYPEREMIA IN RAT GASTRIC-MUCOSA

1 Cholecystokinin octapeptide (CCK-8) and gastrin-17 augment gastric m ucosal blood how in the rat. The present study examined whether the ga stric vasodilator effect of these peptides is mediated by CCKA or CCKB receptors. 2 Intravenous injection of CAM-1481 (1 mg kg(-1)), a dipep toid antagonist of CCKA receptors, or CAM-1028, a dipeptoid CCKB recep tor antagonist (1 mg kg(-1)), had no effect on basal gastric mucosal b lood how as determined by the clearance of hydrogen in urethane-anaest hetized rats. 3 Intravenous infusion of CCK-8 or gastrin-17 (8-200 pmo l min(-1)) increased gastric mucosal blood flow in a dose-dependent fa shion. The CCKB receptor antagonist, CAM-1028, significantly attenuate d the hyperaemic response to CCK-8 and gastrin-17 whereas the CCKA rec eptor antagonist, CAM-1481, did not antagonize CCK-8 but caused a slig ht attenuation of the vasodilator response to gastrin-17. 4 The select ivity of the two antagonists was proved by the findings that CAM-1OZ8, 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, in hibited the CCK-8-induced contraction of guinea-pig isolated gall blad der strips (CCKA receptor assay). 5 These data show that the actions o f CCK-8 and gastrin-17 to increase mucosal blood flow in the rat stoma ch are primarily mediated by CCKB receptors.