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Objective Hydrogen sulfide (H2S) is considered to be a new gaseous molecular alongside with NO and CO.Lots of evidences indicate that H2S performs a wide range of physiological and pathological functions.However, the central cardiovascular effects of H2S are not fully identified.In present study, we tested the hypothesis that H2S in CNS may inhibit NADPH oxidase and decrease the production of ROS, thus mediate central cardiovascular effects.Methods Experiments were completed in Wistar-Kyoto (WKY) rats and spontaneous hypertensive rats (SHR).We used morphological and molecular biological techniques to explore the mechanisms of central cardiovascular effects of H2S.Results The following observations were made: (1) Expressions of CBS of RVLM were increased in WKY rats compared with SHR rats.(2) Intracerebroventricular(ICV) SAM (1 nmol/10 μL) significantly decreased mean arterial pressure (MAP); ICV NaH S by low concentration (4 nmol/10 μL) significantly decreased mean arterial pressure (MAP), while high concentration (20 nmol/10 μL) could increase mean arterial pressure (MAP).(3) Microinjection of NaHS (400 pmol/0.1 μL) into the RVLM notably decreased MAP.(4) The level of ROS in RVLM of SHR rats was higher than WKY rats, and after ICV with NaH S (4 nmol/l0 μL), the level of ROS decreased compared with SHR rats.Moreover, we also certified that the decrease of ROS associated with the inhibition of the activity ofNADPH oxidase.Conclusion The results of present study suggest that H2S in CNS may lower blood pressure by inhibiting the activity of NADPH oxidase in the RVLM in SHR.