Binding of La3+ to Fura-2 can change 340/380 nm fluorescence intensity ratio. Whether La3+ cross ventricular cell membrane was detected by this fluorescent probe technique. Fura-2 loaded isolated guinea pig ventricula...Binding of La3+ to Fura-2 can change 340/380 nm fluorescence intensity ratio. Whether La3+ cross ventricular cell membrane was detected by this fluorescent probe technique. Fura-2 loaded isolated guinea pig ventricular cells were exposed to 0.01-0.1 mM extracellular Lanthanum ion concentration, 340nm/380 nm fluorescence ratio was not changed. Using calcium channel agonist BAY K8644, KCL (35mM) depolarization to open the voltage-dependent calcium channel (VDCC); Adrenoceptor agonist to excite adrenoceptor, 340/380 ratio was not changed, suggesting that La3+can not enter guinea pig ventricular cells in this case.展开更多
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 tha...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.展开更多
文摘Binding of La3+ to Fura-2 can change 340/380 nm fluorescence intensity ratio. Whether La3+ cross ventricular cell membrane was detected by this fluorescent probe technique. Fura-2 loaded isolated guinea pig ventricular cells were exposed to 0.01-0.1 mM extracellular Lanthanum ion concentration, 340nm/380 nm fluorescence ratio was not changed. Using calcium channel agonist BAY K8644, KCL (35mM) depolarization to open the voltage-dependent calcium channel (VDCC); Adrenoceptor agonist to excite adrenoceptor, 340/380 ratio was not changed, suggesting that La3+can not enter guinea pig ventricular cells in this case.
基金the Natural Science Foundation of Hebei Province of China(No.C2007000821)
文摘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.
