Plasma adrenaline is originated from adrenal medulla, while plasma noradrenaline reflects the release from sympathetic nerves in addition to the secretion from adrenal medulla. The present study was designed to characterize the source of plasma catecholamines induced by centrally administered histamine, with regard to the brain prostanoids. Intracerebroventricularly (i.c.v.) administered histamine (1, 5 and 10 μg/animal) elevated plasma noradrenaline and adrenaline (noradrenaline<adrenaline) in a dose-dependent manner. Ketoprofen (a selective inhibitor of cyclooxygenase-1) (100, 250 and 500 μg/animal, i.c.v.) dose-dependently reduced the histamine (5 μg/animal, i.c.v.)-induced elevation of both catecholamines, while NS-398 (a selective inhibitor of cyclooxygenase-2) (250 and 500 μg/animal, i.c.v.) had no effect. The histamine-induced response was dose-dependently attenuated by furegurelate (an inhibitor of thromboxane A₂ synthase) (250 and 500 μg/animal, i.c.v.), and abolished by acute bilateral adrenalectomy. These results suggest that centrally administered histamine evokes plasma noradrenaline and adrenaline from adrenal medulla by brain cyclooxygenase-1- and thromboxane A₂-mediated mechanisms in rats.