Abstract
Several prostanoids were investigated for a potential to induce emesis in Suncus murinus. The TP receptor agonist 11α,9α-epoxymethano-15 S-hydroxyprosta-5 Z,13 E-dienoic acid (U46619) induced emesis at doses as low as 3 μg/kg, i.p. but the DP receptor agonist 5-(6-Carboxyhexyl)-1-(3-cyclohexyl-3-hydroxypropyl) hydantoin (BW245C) was approximately 1000 times less potent. The emetic action of U46619 (300 μg/kg, i.p.) was antagonized significantly by the TP receptor antagonist, vapiprost ( P<0.05). EP (prostaglandin E 2, 17-phenyl-ω-trinor prostaglandin E 2, misoprostol and sulprostone), FP (prostaglandin F 2α and fluprostenol) and IP (iloprost and cicaprost) receptor agonists failed to induce consistent emesis at doses up to 300–1000 μg/kg, i.p. Fluprostenol reduced nicotine (5 mg/kg, s.c.)-but not copper sulphate (120 mg/kg, intragastric)-induced emesis; the other inconsistently emetic prostanoids were inactive to modify drug-induced emesis. The results indicate an involvement of TP and possibly DP and FP receptors in the emetic reflex of S. murinus.
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