17β-estradiol Decreased Late Sodium Current And Reverse Na⁺-Ca²⁺ Exchange Current Via GPER In Ventricular Myocytes

17β-estradiol (E2) could affect a variety of cardiomyocytes ion currents and keepmany kinds of ion concentration in balance. However there were no report about theeffects of E2on late sodium current (INa.L). In this study, whole-cell patch-clamp techniquewas used to explore the effects of E2on normal and H2O2-increased or ATX-induced INa.Land reverse Na+-Ca2+exchange current (reverse INCX). The data showed that E2coulddecrease normal INa.Land reverse INCXin a concentration dependent manner.10nM ATXand300μM H2O2increased INa.Land reverse INCXsignificantly in cardiomyocytes whichwere reversed by100nM E2. cAMP inhibitor H-89or PI3K inhibitor wortmannin (inpipette solution) could not prevent the decreasing effect of E2on INa.L. G-protein coupledestrogen receptor (GPER) agonist G-1inhibited normal INa.Land reverse INCXin aconcentration dependent mode and100nM G-1reversed H2O2-increased or ATX-inducedINa.Land reverse INCXwhich was just the same as E2. In the presence of GPER antagonistG15(40nM),1000nM E2could not decreased INa.L(P>0.05vs40nM G15). Conclusion:E2decreased normal and H2O2-increased or ATX-induced INa.Land reverse INCXvia GPERin ventricular myocytes and these effects may not have a direct relationship with cAMPand PI3K pathways. 17β-estradiol (E2) could affect a variety of cardiomyocytes ion currents and keep manykinds of ion concentration in balance. However there were no report about the effects ofE2on late sodium current (INa.L). In this study, whole-cell patch-clamp technique was usedto explore the effects of E2on normal and H2O2-increased or ATX-induced INa.Landreverse Na+-Ca2+exchange current (reverse INCX). The data showed that E2could decreasenormal INa.Land reverse INCXin a concentration dependent manner.10nM ATX and300μM H2O2increased INa.Land reverse INCXsignificantly in cardiomyocytes which werereversed by100nM E2. cAMP inhibitor H-89or PI3K inhibitor wortmannin (in pipettesolution) could not prevent the decreasing effect of E2on INa.L. G-protein coupled estrogenreceptor (GPER) agonist G-1inhibited normal INa.Land reverse INCXin a concentrationdependent mode and100nM G-1reversed H2O2-increased or ATX-induced INa.Landreverse INCXwhich was just the same as E2. In the presence of GPER antagonist G15(40nM),1000nM E2could not decreased INa.L(P>0.05vs40nM G15). Conclusion: E2decreased normal and H2O2-increased or ATX-induced INa.Land reverse INCXvia GPER inventricular myocytes and these effects may not have a direct relationship with cAMP andPI3K pathways.