The postganglionic sympathetic nerves of the isolated rat stomach were electrically stimulated twice at 1 Hz for 1 min. Prostaglandin E(2) and ONO-AE-248 (16S-9-deoxy-9beta-chloro-15-deoxy-16-hyfroxy-17,17-trimethylene-19,20-didehydro prostaglandin F(2)) (an EP(3) receptor agonist) reduced the evoked noradrenaline release, while ONO-DI-004 (17S-2,5-ethano-6-oxo-17,20-dimethyl prostaglandin E(1)) (an EP(1) receptor agonist), ONO-AE1-259-01 (11,15-O-dimethyl prostaglandin E(2)) (an EP(2) receptor agonist) and ONO-AE1-329 [16-(3-methoxymethyl)phenyl-omega-tetranor-3,7-dithia prostaglandin E(1)] (an EP(4) receptor agonist) had no effect. U-46619 (9,11-dideoxy-9alpha,11alpha-methanoepoxy prostaglandin F(2alpha)) and I-BOP (7-[3-[3-hydroxy-4-(4-iodophenoxy)-1-butenyl]-7-oxabicyclo[2,2,1] hept-2-yl]-,[1S[1alpha,2alpha(Z),3beta(1E,3S)4alpha]]-5-heptenoic acid) (TP receptor agonists) also reduced the noradrenaline release and these inhibitory effects were abolished by SQ-29548 (7-[3-[[2-[(phenylamino) carbonyl] hydrazino]methyl]-7-oxabicyclo[2,2,1]hept-2-yl][1S(1alpha,2alpha(Z), 3alpha,4alpha]-5-heptenoic acid) (a TP receptor antagonist). The inhibitory effect of U-46619, but not ONO-AE-248, was abolished by pertussis toxin. These results suggest that the prostanoid EP(3) and TP receptors mediate the inhibition of gastric noradrenaline release; TP, but not EP(3), receptor-mediated inhibition is mediated by a pertussis toxin-sensitive mechanism in rats.