1. Acetylcholine (10 micrograms/min) diminished the electrically-induced cerebral blood flow reductions. Atropine (1-2 mg) partially blocked this inhibitory effect. 2. Exogenously administered noradrenaline (1-10 micrograms) and tyramine (50-500 micrograms) reduced cerebral blood flow but this effect was unchanged by acetylcholine infusion. 3. Acetylcholine inhibited the nonadrenergic component of the electrically-induced contraction at a concentration greater than or equal to 10(-6) M and potentiated the adrenergic component at a concentration greater than or equal to 10(5) M. Atropine 10(-7) M) inhibited both of these effects. In addition, acetylcholine (10(-4) M) enhanced the electrically-evoked [3H]noradrenaline overflow. 4. These results show that: (a) acetylcholine modulates cerebrovascular sympathetic neurotransmission by acting on muscarinic receptors; and (b) the potentiating effect of acetylcholine is achieved by a mechanism involving increases in noradrenaline release.