1. 1. Field electrical stimulation induced tritium release from cat cerebral arteries preincubated with [3H]serotonin (5-HT). 2. 2. This release was markedly reduced by tetrodotoxin (0.8 μM), B-HT 920 (1 μM), denervation with 6-OH-dopamine (6-OHDA) and OCa2+, and increased by phentolamine (1 μM) and phorbol 12,13-dibutyrate (1 and 3 μM). 3. 3. 5-HT (10 and 100 μM) and NA (0.1, 1 and 10 μM) caused concentration-dependent tritium release in control arteries, but not in those denervated with 6-OHDA. 4. 4. [3H]5-HT uptake was greatly reduced by preincubation of arteries with cocaine (10 μM), ouabain (100 μM) or denervation with 6-OHDA. 5. 5. 5-HT did not amplify contractions elicited by noradrenaline (NA) in middle cerebral arteries. 6. 6. These data indicate: (1) 5-HT is mainly accumulated in adrenergic nerve endings; (2) 5-HT release is modulated by presynaptic α2-adrenoceptors; (3) protein kinase C of perivascular adrenergic nerve endings participates in 5-HT release, and (4) 5-HT did not amplify NA responses. © 1990.