S U M M A R Y The responses of baboon cerebral and extracerebral arteries to prostaglandin endoperoxide (PGH2) and prostacyclin (PGI2) were investigated on isolated arteries and in vivo by serial angiography. Both PGH2 and PGI2 could produce dose-dependent contraction or relaxation of isolated arteries. PGH2 induced relaxation was indicative of prostacyclin synthetase activity, the enzyme which converts PGH2 to PGI2. In isolated arteries tested one to four hours post mortem only the vertebral artery showed prostacyclin synthetase activity. Thus PGH2 induced contraction of cerebral arteries may be indicative of a physiological function. Vasomotor tone may in part be the result of a balance between PGH2 constriction and PGI2 dilatation. In vivo PGI2 infusion caused pronounced and prolonged dilatation of cerebral arteries, which lasted longer than the cardiovascular changes. As PGI2 is the most potent cerebral vasodilator drug tested, it may be of clinical use in the treatment of cerebral vasospasm.Prostacyclin is a recently discovered prostaglandin with potent vasodilator effects on peripheral and central blood vessels. In addition prostacyclin is one of the most potent inhibitors of platelet aggregation known. The potential therapeutic applications of the use of this drug or more stable analogues is currently under study (Moncada and Vane, 1978).In view of its potent relaxing actions on human and baboon cerebral arteries (Boullin et al., 1979) prostacyclin may be of use in the prevention or reversal of cerebral arterial vasospasm which commonly occurs after the rupture of aneurysms of the major cerebral arteries.Before any clinical studies it is of course necessary to examine the actions of prostacyclin and precursors (prostaglandin endoperoxides, PGG2, PGH2) upon the cerebral vasculature of animals.For some years we have been using the baboon as a model for studying the aetiology of human vasospasm (see Boullin et al., 1977.