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We examined the hypothesis that oxygen radicals may mediate the vasodilator effect of VIP on cerebral arterioles in cats equipped with cranial windows. The appearance of superoxide anion radical in cerebral extracellular space during VIP application was examined by measuring the rate of superoxide dismutase (SOD)-inhibitable reduction of nitroblue tetrazolium (NBT). Although VIP (1 and 10 micrograms/ml) caused substantial reduction of NBT, the rate of the SOD-inhibitable portion was not significantly different from zero. We also examined the effect of scavenging of superoxide and hydrogen peroxide by topical application of SOD plus catalase on the vasodilator effect of VIP (0.05-1.0 microgram/ml). The dilation in response to VIP was not significantly affected in either large or small arterioles by scavenging of superoxide and hydrogen peroxide. We conclude that VIP does not cause generation of superoxide and that superoxide or other reactive oxygen species derived from it, such as hydrogen peroxide and hydroxyl radical, are not mediators of the cerebral vasodilation caused by VIP.

Superoxide anion radical does not mediate vasodilation of cerebral arterioles by vasoactive intestinal polypeptide.