Ondansetron (10 mgkg, p.0.) and granisetron (1 mgkg, p.0.) also inhibited the stress-accelerated colonic transit, but azasetron was more effective than these two drugs. Atropine methylbromide (0.1 mg/kg, s .~) and tetrodotoxin (0.01 mg/kg, s.c.) inhibited the accelerated colonic transit under stress conditions, but methysergide (10 mgkg, s.c.), SDZ205-557 (10 mg/kg, s.c.), domperidone (30 mgkg, P.o.), trimebutine (300 mgkg, P.o.), and metoclopramide (30 mgkg, p.0.) did not. Azasetron (10 pg) administered intracerebroventricularly did not inhibit the stressinduced acceleration. These results suggest that endogenous 5-HT which is released through stress accelerates the colonic transit via the 5-HT3 receptors and finally a cholinergic mechanism. It is considered that azasetron inhibits colonic transit partic- ularly under stress conditions through the blockade of the peripheral 5-HT3 receptors. Azasetron may improve bowel function in strewrelated colonic dysfunction like irritable bowel syndrome.