The present study was aimed to identify whether endogenously produced nitric oxide (NO) plays a role in preservation of cerebral blood flow (CBF) autoregulation in rat pial artery during the acute stage after subarachnoid haemorrhage (SAH). During the acute stage after SAH, the lower limit of CBF autoregulation significantly shifted to the higher arterial blood pressure in association with suppressed vasodilatation in response to acute hypotension, which was accompanied by significantly increased expression of endothelial nitric oxide synthase mRNA and increased production of superoxide anion in cerebral vessels. SAH-induced increase in superoxide production was further enhanced under pretreatment with N-nitro-L-arginine methyl ester in the cerebral vessels. Following additional administration of L-arginine (100 mg/kg, i.p.), the haemodynamic alterations were significantly restored in association with significantly reduced superoxide level in the cerebral vessels. In line with these findings, rats that received polyethylene glycol superoxide dismutase and catalase or Mn(III) tetrakis (4-benzoic acid) porphyrin chloride showed recovery of impaired autoregulatory vasodilation in response to acute hypotension. Thus, it is suggested that NO endogenously produced is importantly implicated in the preservation of CBF autoregulation during the acute stage after SAH via its capability to scavenge superoxide anion.