Gomez Carolina B, Sánchez-López Araceli, Carvajal Karla, Centurión David
Departamento de Farmacobiología, Cinvestav-Coapa, Czda. de Los Tenorios 235, Col. Granjas-Coapa, Alc. Tlalpan, C.P. 14330, Ciudad de México, Mexico.
Laboratorio de Nutrición Experimental, Instituto Nacional de Pediatría, Insurgentes Sur 3700 Letra C, Alc. Coyoacán, C.P. 04530, Ciudad de México, Mexico.
Int J Hypertens. 2024 Nov 4;2024:5848352. doi: 10.1155/2024/5848352. eCollection 2024.
Elevated blood pressure is the leading metabolic risk factor in attributable deaths, and hydrogen sulfide (HS) regulates vascular tone and blood pressure. Thus, this study aims to evaluate the mechanism by which NaHS (HS 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 channel blocker, 5 mg/kg), (3) barium chloride (BaCl, K channel blocker, 65 g/kg), (4) saline solution (vehicle of TEA, 4-AP, and BaCl, 1 mL/kg), (5) glibenclamide (K channel blocker, 10 mg/kg), and (6) glibenclamide vehicle (DMSO + glucose 10% + NaOH, 1 mL/kg), and then a 310 g/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 channel blocker, BaCl, in obese rats. The above data suggest that the potassium channel could be involved in the sympathoinhibition induced by NaHS.
血压升高是可归因死亡中的主要代谢风险因素，而硫化氢（HS）可调节血管张力和血压。因此，本研究旨在评估硫氢化钠（HS供体）抑制肥胖大鼠血管升压交感神经输出的机制。为此，给动物喂食高脂饮食（HFD）（60%的热量来自脂肪），持续12周。对它们进行麻醉、毁髓并插管，以评估钾通道在硫氢化钠诱导的交感神经抑制中的作用。动物接受血管升压交感神经输出的选择性电刺激，并静脉注射（i.v.）：（1）四乙铵（TEA，非选择性钾通道阻滞剂，16.5mg/kg）、（2）4-氨基吡啶（4-AP，钾通道阻滞剂，5mg/kg）、（3）氯化钡（BaCl，钾通道阻滞剂，65g/kg）、（4）盐溶液（TEA, 4-AP和BaCl的载体，1mL/kg）、（5）格列本脲（钾通道阻滞剂，10mg/kg），以及（6）格列本脲载体（二甲亚砜+10%葡萄糖+氢氧化钠，1mL/kg），然后以310g/kg·min的速度静脉持续输注硫氢化钠。我们观察到：（1）硫氢化钠可抑制血管升压交感神经输出；（2）在肥胖大鼠中，钾通道阻滞剂氯化钡可逆转硫氢化钠的交感神经抑制作用。上述数据表明，钾通道可能参与了硫氢化钠诱导的交感神经抑制过程。
