Effect of Hydrogen Sulfide on Sympathoinhibition in Obese Pithed Rats and Participation of K⁺ Channel

Elevated blood pressure is the leading metabolic risk factor in attributable deaths, and hydrogen sulfide (H₂S) regulates vascular tone and blood pressure. Thus, this study aims to evaluate the mechanism by which NaHS (H₂S donor) produces inhibition of the vasopressor sympathetic outflow in obese rats. For that purpose, animals were fed a high-fat diet (HFD) (60% calories from fat) for 12 weeks. They were anesthetized, pithed, and cannulated to evaluate the role of the potassium channel on NaHS-induced sympathoinhibition. Animals received selective electrical stimulation of the vasopressor sympathetic outflow, an intravenous (i.v.) administration of (1) tetraethylammonium (TEA, non-selective K⁺ channel blocker, 16.5 mg/kg), (2) 4-aminopyridine (4-AP, K_V channel blocker, 5 mg/kg), (3) barium chloride (BaCl₂, K_IR channel blocker, 65 μg/kg), (4) saline solution (vehicle of TEA, 4-AP, and BaCl₂, 1 mL/kg), (5) glibenclamide (K_ATP channel blocker, 10 mg/kg), and (6) glibenclamide vehicle (DMSO + glucose 10% + NaOH, 1 mL/kg), and then a 310 μg/kg·min NaHS i.v. continuous infusion. We observed that (1) NaHS produced inhibition of the vasopressor sympathetic outflow and (2) the sympathoinhibitory effect by NaHS was reversed by the K_IR channel blocker, BaCl₂, in obese rats. The above data suggest that the potassium channel could be involved in the sympathoinhibition induced by NaHS.