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Aim: The present study was to define the effect of H2S on central region which regulates sympathetic outflow by perfusion of isolated carotid sinus with H2S.Methods: Sodium hydrogen sulfide (NaHS), a H2S donor,was perfused into isolated carotid sinus;the functional curve of the carotid sinus baroreflex was measured by recording changes in renal sympathetic nerve activity (RSNA) in anesthetized male rats.Results: (1) Perfusion of isolated carotid sinus with NaHS (25, 50, and 100 μmol/L) dose-dependently inhibited sympathetic outflow by enhancing the response of RSNA to the increased intrasinus pressure (ISP).RSNA was decreased to 84.95 ±3.58% (P<0.01), 63.89 ± 2.53% (P<0.01) and 48.70 ± 4.16%(P<0.01) compare with control.(2) Pretreatment with glibenclamide (20 μmol/L), a KATP channels blocker, the above effect of NaHS was abolished.(3) Prior perfusion of Bay K8644 (500 nmol/L), an agonist of calcium channels, the effect of NaHs was eliminated.(4) Perfusion of the cystathionine γ-lyase (CSE) inhibitor, DL-propargylglycine (PPG, 200 μmol/L) increased sympathetic outflow.Conclusion: The results suggest that perfusion of isolated carotid sinus with NaHS inhibits sympathetic outflow as evidenced by the decrease of RSNA.The effect is mediated by opening a KATP channels and further closing the calcium channel in smooth muscle cells.Endogenous H2S may tonically suppress the sympathetic vasomotor by activating the activity of the carotid sinus baroreflex (CSB).