ACh usually induced biphasic vascular responses, i.e. an initial vasodilation followed by a secondary constriction, in isolated and perfused basilar arteries from the dog. In dog vessels the vasoconstriction induced by ACh was not modified by treatment with phentolamine, at dose levels which suppressed noradrenaline-induced constriction, but was completely blocked by atropine. The dilation to ACh was also blocked by atropine. Physostigmine caused a potentiation of both ACh-induced dilator and constrictor responses. In dogs, ACh-induced constrictor responses were markedly potentiated, and the vasodilatation was slightly but insignificantly enhanced after treatment with intraluminal saponin which removed the endothelia of the arteries. In basilar arteries from monkeys, ACh usually induced a monophasic vasoconstriction in non-treated preparations. In monkey vessels, ACh-induced vasoconstriction was markedly potentiated and frequently vasodilatation appeared after intraluminal saponin treatment. From these results, it is concluded that ACh has primary vasoconstrictor and vasodilator properties in canine and simian cerebral basilar arteries.