1. The changes on blood pressure induced by pharmacological handling of serotonergic systems were studied in normotensive anesthetized rats. Administration of 5-hydroxytryptophan (5-HTP) (5, 10 and 30 mg/kg i.v.) produced a dose-dependent decrease in mean blood pressure without significative effect on heart rate. 2. Inhibition of either peripheral L-aminoacid DOPA decarboxylase or monoamine oxydase enzymes increased this hypotensive effect. 3. Methysergide, a serotonergic antagonist, prevented the hypotension induced by 5 OH-TP in animals whose peripheral decarboxylase was inhibited. 4. Fenfluramine, a serotonergic releasing drug, produced a decrease in both blood pressure and heart rate. These effects were prevented by inhibiting fenfluramine uptake or by serotonin (5-HT) receptor blockade. 5. The hypotensive action induced by 5-HTP was not affected when opioid, dopaminergic or histaminergic receptors were blocked. 6. In animals injected intracisternally with a serotonergic neurotoxine a selective destruction of serotonergic terminals of spinal cord was obtained. 7. In these animals the dose-response curve relating hypotensive effect induced by a direct serotonergic agonist showed a significative shift to the left when compared with control group, suggesting the existence of supersensitivity. 8. Our results show that increases in central serotonergic activity produce a hypotensive effect in normotensive anesthetized rats. The receptor involved in this action could be localized in spinal cord.