P52 Perfusion of isolated carotid sinus with hydrogen sulfide attenuated the renal sympathetic nerve activity in anesthetized male rats

Abstract

The present study was to define the effect of H 2 S on central region which regulates sympathetic outflow by perfusion of isolated carotid sinus with H 2 S. Sodium hydrogen sulfide (NaHS), a H 2 S 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. (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 K ATP 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. 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 K ATP channels and further closing the calcium channel in smooth muscle cells. Endogenous H 2 S may tonically suppress the sympathetic vasomotor by activating the activity of the carotid sinus baroreflex (CSB).