CENTRAL AND NO-MEDIATED MECHANISMS ARE INVOLVED IN THE INHIBITORY EFFECTS OF CCK ON THE CHICKEN CECORECTAL AREA

In chickens CCK-8s induces defecation and causes an inhibition of rect al electrical activity (EA) and an increase in cecal motility. In cont rast, CCK-4 inhibits the motility of both rectum and ceca. The cecorec tal responses to CCK-8s and CCK-4, given intravenously (i.v.), were st udied in conscious chickens prepared with electrodes for electromyogra phy; the influence of atropine, phentolamine plus propranolol, hexamet honium and L-NAME on such responses was determined. Atropine and phent olamine plus propranolol did not cause any change in the response to C CK-8s or CCK-4 in the cecorectal area. Hexamethonium only induced a si gnificant decrease in the number of defecations (ND) induced by CCK-8s . L-NAME slightly modified the decrease in rectal EA due to CCK-8s. Th e effects of intracerebroventricular (i.c.v.) administration of CCK-8s and CCK-4 were also studied. CCK-8s and CCK-4, given i.c.v., caused, in conscious chickens, a slight decrease in cecal EA, in the 15 minute s following administration. This effect was similar to that seen after i.v. administration of CCK-4. In conclusion, our results suggest that the inhibitory action of CCK on chicken rectum is mediated, at least in part, through nitric oxide release. In addition, nicotinic receptor s mediate the increase in the ND caused by CCK-8s. Ganglionic, muscari nic, adrenergic and nitrergic blockade were not able to modify the exc itatory cecal response to CCK-8s, which may indicate that the receptor mediating this effect is located on the cecal smooth muscle. Finally, the inhibitory action of i.v. CCK-4 on chicken cecum seems to be cent rally mediated, as suggested by the fact that i.c.v. administration of either CCK-8s or CCK-4 induce a similar effect.