Intraventricular administration of histamine (HA; 2.5 and 5 micrograms) caused a significant increase of plasma adrenaline and noradrenaline levels in conscious, freely-moving male rats. The increase of adrenaline was more rapid (5 min after injection) and greater than that of noradrenaline. The plasma adrenaline increase observed 15 min after HA administration was dose-dependent. In contrast, plasma noradrenaline increased maximally in response to the low dose and reached similar values after the largest dose studied. Receptor mediation was examined by means of selective HA antagonists. Pretreatment with mepyramine blunted the adrenaline response at 15 min which suggests mediation at H1 receptors. In contrast, it was ineffective on plasma adrenaline at 5 min and plasma noradrenaline increase. Ranitidine, an H2-receptor antagonist, did not modify adrenaline response but enhanced the HA-induced increase of plasma noradrenaline. These findings suggest that HA activates the central drive to the adrenal medulla and to the peripheral sympathetic system. A participation of peripheral catecholamine secretion in the acute cardiovascular changes induced in rats by centrally injected HA is postulated.