Several prostanoids were investigated for their ability to induce emesis and/or defecation and tenesmus in the ferret. The rank order of emetic potency (dose producing four episodes, D 4 ) was: sulprostone (5 μg/kg)>11α,9α-epoxymethano-15S-hydroxyprosta-5Z,13E-dienoic acid (U46619; 8 μg/kg)>misoprostol (27 μg/kg)>17-phenyl-ω-trinor prostaglandin E 2 (53 μg/kg)>prostaglandin E 2 (94 μg/kg)>5-(6-carboxyhexyl)-1-(3-cyclohexyl-3-hydroxypropyl) hydantoin (BW245C; 148 μg/kg)≫prostaglandin F 2α (13,500 μg/kg). Emesis was also induced by iloprost (D 4 not determined) and prostaglandin E 2 methyl ester (D 4 =350 μg/kg). Cicaprost and fluprostenol were virtually inactive; they also failed to modify copper sulphate (100 mg/kg, intragastric)-induced emesis (P>0.05), although cicaprost potentiated apomorphine (0.25 mg/kg, s.c.)-induced emesis (P<0.05). U46619-induced emesis was antagonised by vapiprost (P<0.05). The rank order of potency to produce defecation and tenesmus (dose producing three episodes) was: sulprostone (12 μg/kg)>misoprostol (15 μg/kg)>17-phenyl-ω-trinor prostaglandin E 2 (94 μg/kg)>prostaglandin E 2 (113 μg/kg)>fluprostenol (158 μg/kg)≫prostaglandin F 2α (1759 μg/kg); prostaglandin E 2 methyl ester also induced defecation (196 μg/kg). Data are discussed in relation to mechanisms involved in emesis and defecation.