Abstract
Elevated blood pressure is the leading metabolic risk factor in attributable deaths, and hydrogen sulfide (H(2)S) regulates vascular tone and blood pressure. Thus, this study aims to evaluate the mechanism by which NaHS (H(2)S 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 (BaCl(2), K(IR) channel blocker, 65 μg/kg), (4) saline solution (vehicle of TEA, 4-AP, and BaCl(2), 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, BaCl(2), in obese rats. The above data suggest that the potassium channel could be involved in the sympathoinhibition induced by NaHS.