Guo Q, Wu Y, Xue H, Xiao L, Jin S, Wang R
Department of Physiology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang, China.
Physiol Res. 2016 Jul 18;65(3):413-23. doi: 10.33549/physiolres.933050. Epub 2016 Mar 15.
The purpose of the present study was to define the indirect central effect of hydrogen sulfide (H(2)S) on baroreflex control of sympathetic outflow. Perfusing the isolated carotid sinus with sodium hydrosulfide (NaHS), a H(2)S donor, the effect of H(2)S was measured by recording changes of renal sympathetic nerve activity (RSNA) in anesthetized male rats. Perfusion of isolated carotid sinus with NaHS (25, 50, 100 micromol/l) dose and time-dependently inhibited sympathetic outflow. Preconditioning of glibenclamide (20 micromol/l), a ATP-sensitive K(+) channels (K(ATP)) blocker, the above effect of NaHS was removed. With 1, 4-dihydro-2, 6-dimethyl-5-nitro-4-(2-[trifluoromethyl] phenyl) pyridine-3-carboxylic acid methyl ester (Bay K8644, 500 nmol/l) pretreatment, which is an agonist of L-calcium channels, the effect of NaHS was eliminated. Perfusion of cystathionine gamma-lyase (CSE) inhibitor, DL-propargylglycine (PPG, 200 micromol/l), increased sympathetic outflow. The results show that exogenous H(2)S in the carotid sinus inhibits sympathetic outflow. The effect of H(2)S is attributed to opening K(ATP) channels and closing the L-calcium channels.
本研究的目的是确定硫化氢（H₂S）对压力反射控制交感神经传出的间接中枢效应。用硫化氢供体硫氢化钠（NaHS）灌注离体颈动脉窦，通过记录麻醉雄性大鼠肾交感神经活动（RSNA）的变化来测量H₂S的作用。用NaHS（25、50、100微摩尔/升）灌注离体颈动脉窦，剂量和时间依赖性地抑制交感神经传出。用格列本脲（20微摩尔/升）预处理，它是一种ATP敏感性钾通道（KATP）阻滞剂，可消除NaHS的上述作用。用L型钙通道激动剂1,4-二氢-2,6-二甲基-5-硝基-4-(2-[三氟甲基]苯基)吡啶-3-羧酸甲酯（Bay K8644，500纳摩尔/升）预处理，可消除NaHS的作用。灌注胱硫醚γ-裂解酶（CSE）抑制剂DL-炔丙基甘氨酸（PPG，200微摩尔/升）可增加交感神经传出。结果表明，颈动脉窦中的外源性H₂S抑制交感神经传出。H₂S的作用归因于开放KATP通道和关闭L型钙通道。
