Hydrogen sulfide facilitates carotid sinus baroreceptor activity in anesthetized male rats  

作　　者：XIAO Lin WU Yu-ming WANG Ru LIU Yi-xian WANG Fu-wei HE Rui-rong 

机构地区：[1]Department of Physiology, Institute of Basic Medicine, Hebei Medical Univesity, Shijiazhuang 050017, China

出　　处：《Chinese Medical Journal》2007年第15期1343-1347,共5页中华医学杂志（英文版）

基　　金：the Natural Science Foundation of Hebei Province of China(No.C2007000821)

摘　　要：Background It has been reported that hydrogen sulfide （H2S） could relax vascular smooth muscle by direct activation of KATP channels and hyperpolarization of the membrane potential. Recently, our study has shown that H2S facilitated carotid baroreflex. This study was conducted to investigate the effect of H2S on carotid baroreceptor activity （CBA）. Methods The functional curve of carotid baroreceptor （FCCB） was constructed and the functional parameters of carotid baroreceptor were measured by recording sinus nerve afferent discharge in anesthetized male rats with perfused isolated carotid sinus. Results H2S （derived from NariS） 25, 50 and 100 pmol/L facilitated CBA, which shifted FCCB to the left and upward. There was a marked increase in peak slope （PS） and peak integral value of carotid sinus nerve charge （PIV） in a concentration-dependent manner. Pretreatment with glibenclamide （20 pmol/L）, a KATP channel blocker, the above effects of H2S on CBA were abolished. Pretreatment with Bay K8644 （an agonist of calcium channels, 500 nmol/L） eliminated the role of H2S on CBA. An inhibitor of cystathionine y-lyase （CSE）, DL-propargylglycine （PPG, 200 pmol/L） inhibited CBA in male rats and shifted FCCB to the right and downward. Conclusions Our results suggest that exogenous H2S exerts a facilitatory role on isolated CBA through opening KATP channels and further closing the calcium channels in vascular smooth muscle. Endogenous H2S may activate CBA in vivo.Background It has been reported that hydrogen sulfide （H2S） could relax vascular smooth muscle by direct activation of KATP channels and hyperpolarization of the membrane potential. Recently, our study has shown that H2S facilitated carotid baroreflex. This study was conducted to investigate the effect of H2S on carotid baroreceptor activity （CBA）. Methods The functional curve of carotid baroreceptor （FCCB） was constructed and the functional parameters of carotid baroreceptor were measured by recording sinus nerve afferent discharge in anesthetized male rats with perfused isolated carotid sinus. Results H2S （derived from NariS） 25, 50 and 100 pmol/L facilitated CBA, which shifted FCCB to the left and upward. There was a marked increase in peak slope （PS） and peak integral value of carotid sinus nerve charge （PIV） in a concentration-dependent manner. Pretreatment with glibenclamide （20 pmol/L）, a KATP channel blocker, the above effects of H2S on CBA were abolished. Pretreatment with Bay K8644 （an agonist of calcium channels, 500 nmol/L） eliminated the role of H2S on CBA. An inhibitor of cystathionine y-lyase （CSE）, DL-propargylglycine （PPG, 200 pmol/L） inhibited CBA in male rats and shifted FCCB to the right and downward. Conclusions Our results suggest that exogenous H2S exerts a facilitatory role on isolated CBA through opening KATP channels and further closing the calcium channels in vascular smooth muscle. Endogenous H2S may activate CBA in vivo.

关 键 词：hydrogen sulfide potassium channels GLIBENCLAMIDE BARORECEPTORS Bay K8644 

分 类 号：R614[医药卫生—麻醉学]