Hydroperoxide-induced oxidative stress is assumed to be involved in vasospasm of cerebral arteries after subarachnoid hemorrhage. In order to study underlying mechanisms the effects of H2O2 and tert butylhydroperoxide on contractile functions as well as on free radical production of anterior cerebral artery from pig were investigated. The hydroperoxides increased in a similar dose-dependent arterial contraction, however, the underlying mechanisms involve impairment of endothelial-dependent relaxation as well as of smooth muscle contractile function as shown by experiments with inhibited endothelial NO-synthesis. Determination of lucigenine detectable O2(-)-release showed rather low values with both hydroperoxides, whereas, in comparison, the unspecific luminol-dependent chemi-luminescence was increased up to 1000-fold, especially by H2O2. In conclusion it was shown that application of the hydroperoxides resulted in increased contraction of cerebral arteries, yet that the underlying mechanisms altering function of endothelial and smooth muscle cells need further exploration.