雌二醇对家兔窦房结自律细胞的电生理学效应(英文)

Electrophysiologic effects of 17 β-estradiol on pacemaker cells in sinoatrial nodes of rabbits

本文旨在探讨雌二崞(17β-estradiol)对家兔窦房结自律细胞的电生理学效应及其作用机制。应用经典的细胞内玻璃微电极技术观察不同浓度雌二醇(1,10,100μmol/L)对家兔窦房结自律细胞动作电位的影响。结果显示:(1)雌二醇浓度依赖性地延长窦房结自律细胞动作电位复极化50%时间(APD_(50))和动作电位复极化90%时间(APD_(90)),降低窦房结自律细胞动作电位0期最大除极速率(V_(max))、动作电位幅值(amplitude of action potential,APA),降低窦房结自律细胞放电频率(rate of pacemaker firing.RPF)、舒张期(4相)自动去极化速率[velocity of diastolic(phase 4)depolarization,VDD];而雌二醇对窦房结自律细胞的最大舒张电位(maximal diastolic potential,MDP)无明显影响。(2)雌激素受体阻断剂他莫昔芬(10μmol/L)不能阻断雌二醇(10μmol/L)对窦房结自律细胞动作电位的抑制效应(3)一氧化氮合酶抑制剂L-NAME(100μmol/L)可完全阻断雌二醇(10μmol/L)对窦房结自律细胞动作电位的抑制效应。结果提示,雌二醇对家兔窦房结自律细胞的电生理活动具有明显的抑制作用,此作用可能是通过非基因组机制发挥,与一氧化氮作用有关。

To investigate the electrophysiological effects of 17β-estradiol on pacemaker cells in sinoatrial （SA） nodes of rabbits and the underlying mechanism, intracellular microelectrode technique was used to record action potential （AP） in SA node cells of rabbits. The results showed that： （1） 17β-estradiol （1, 10, 100 μmol/L） not only significantly decreased the amplitude of action potential （APA） and the maximal rate of depolarization （Vmax）, but also decreased the velocity of diastolic （phase 4） depolarization （VDD） and rate of pacemaker firing （RPF） in a concentration-dependent manner. The AP duration at 50% repolarization （APD50） and at 90% repolarization （APDg0） were prolonged. But the maximal diastolic potential （MDP） was not affected. （2） Pretreatment with tamoxifen （10 μmol/ L）, an inhibitor of estrogen receptor, did not block the electrophysiological effects of 17β-estradiol （10 μmol/L） on SA node cells. （3） Pretreatment with N^G-nitro-L-arginine methyl ester （L-NAME, 100 μmol/L）, a nitric oxide （NO） synthase inhibitor, completely abolished the electrophysiological effects of 17β-estradiol （10μmol/L） on SA node cells. The results suggest that 17β-estradiol inhibits the electrophysiological activity of pacemaker cells in SA nodes of rabbits in a concentration-dependent manner possibly through a nongenomic mechanism related with NO.