The effects of 3-morpholinosydnonimine (SIN-1) were studied in isolated canine basilar arteries. Rings with and without endothelium were suspended in Krebs-Ringer bicarbonate solution bubbled with 95% O2-5% CO2. Changes in isometric force were recorded. SIN-1, nitric oxide, and sodium nitroprusside caused concentration-dependent relaxations of control preparation contracted by uridine-5'-triphosphate. The removal of endothelium augmented the relaxation to the nitrovasodilators. Increasing concentrations of SIN-1 reduced endothelium-dependent contractions to the calcium ionophore A23127 and arachidonic acid. The results of the present study suggest that SIN-1 causes relaxation and prevents endothelium-dependent contractions in cerebral arteries. The inhibitory effect of SIN-1 is reduced by the presence of endothelium possibly by interaction with endothelium-derived relaxing factors and/or superoxide anions produced in endothelial cells. The inhibition of endothelium-dependent contractions could be due in part to chemical interactions between endothelium-derived contracting factor (superoxide anion) and the nitric oxide liberated by SIN-1.