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To determine the effect and mechanisms of endogenous hydrogen sulfide(H2S)on reactive oxygen species(ROS)induced by angiotensin Ⅱ(Ang Ⅱ)in medullary neurons.Primary cultured rat medullary neurons were employed for the study.Identification of medullary neurons and cystathionine β-synthetase(CBS)-an enzyme that generated endogenous H2S co-expression were detected by double-labeling immunofluorescence.Medullary neurons were treated with Ang Ⅱ in the presence or absence of NaBu(sodium butyrate,a CBS agonist,100 μmol/L,250 μmol/L and 500 μmol/L).ROS production was measured with dihydroethidium(DHE)staining.The activity of total superoxide dismutase(SOD)was detected by Elisa kit.The expression of CBS mRNA was determined by real-time PCR.(1)90%of our cultured cells were medullary neurons.Ang Ⅱ(1 μmol/L)significantly increased ROS level in medullary neurons;(2)Ang Ⅱ inhibited activity of total SOD in medullary neurons;(3)CBS was expressed in medullary neurons and the expression of CBS mRNA was decreased by Ang Ⅱ;(4)NaBu(250 μmol/L and 500 μmol/L)inhibited ROS induced by Ang Ⅱ significantly with a dose-dependent manner,while NaBu alone had no influence on the ROS level of medullary neurons.Our present study indicates that ROS production induced by Ang Ⅱ in medullary neurons partially by decreasing activity of total SOD and CBS mRNA,while endogenous H2S may inhibit Ang Ⅱ-induced ROS via the opposite effect.