CAJ | 학술논문

目的研究雌激素对豚鼠心室肌细胞的非基因组作用.方法方法采用全细胞膜片钳技术.结果17β-雌二醇1 μmol/L和3 μmol/L在1～2 min内快速抑制INa峰值,抑制率分别13.25%±4.71%,32.46%±4.82%.1 μmol/L 17β-雌二醇亦可影响INa的电流-电压(I-V)曲线,使INa电流密度值在-30mV～+30 mV膜电位下显著降低.在-20 mV处,INa电流密度值由-120.48±7.05 pA/pF降至-101.91±11.00pA/pF(P＜0.01).在+30 mV处,INa电流密度值由-39.55±10.50pA/pF降至-29.88±6.21pA/pF(P＜0.05).17β-雌二醇的抑制效应被DNA转录抑制剂-放线菌素D所阻断.且抑制效应与豚鼠的性别无关.结论雌激素通过推测的非基因组效应快速抑制豚鼠心室肌细胞钠电流(INa),且该效应不被放线菌素D所阻断.
목적연구자격소대돈서심실기세포적비기인조작용.방법방법채용전세포막편겸기술.결과17β-자이순1 μmol/L화3 μmol/L재1～2 min내쾌속억제INa봉치,억제솔분별13.25%±4.71%,32.46%±4.82%.1 μmol/L 17β-자이순역가영향INa적전류-전압(I-V)곡선,사INa전류밀도치재-30mV～+30 mV막전위하현저강저.재-20 mV처,INa전류밀도치유-120.48±7.05 pA/pF강지-101.91±11.00pA/pF(P＜0.01).재+30 mV처,INa전류밀도치유-39.55±10.50pA/pF강지-29.88±6.21pA/pF(P＜0.05).17β-자이순적억제효응피DNA전록억제제-방선균소D소조단.차억제효응여돈서적성별무관.결론자격소통과추측적비기인조효응쾌속억제돈서심실기세포납전류(INa),차해효응불피방선균소D소조단.
Objective The aim of this study was to investigate the nongenomic effect of estrogen in guinea-pig ventricular myocytes. Methods The whole-cell patch-clamp recording technique was used. Results 17β-estradiol 1 μmol/L and 3 μmol/L could, within 1-2 min, rapidly decreased the peak amplitude of INa by 13.25% ±4.71%, (n =7, P ＜0.01), 32.46% ±4. 82% (n =6, P＜0. 01 ) respectively. Current-Voltage curve of sodium current was shifted to upside by 1 μmol/L17β-estradiol. The maximal inhibitory effect of 1 μmol/L 17β-estradiol on INa appeared near -20mV, and the INa density was decreased from - 120. 48 ±7.05 pA/pF to - 101.91 ± 11.00pA/pF(P ＜0. 01 ). At +30 mV, a significant difference still existed in INa density between control ( -39.55 ± 10. 50pA/pF) and 17β-estradiol ( - 29.88 ± 6.21 pA/pF) (P ＜ 0. 05 ). The inhibitory effect of 17 β-estradiol on INa density was not blocked by pretreatment with actinomycin D, an inhibitor of DNA transcription ( n = 12, P ＞0. 05 ). There was no difference in the rapid inhibitory effect of 17β-estradiol on INa between male and female guinea-pigs ( n = 12, P ＞ 0. 05 ). Conclusion Estrogen could rapidly suppress guinea-pig ventricular myocytes INa by a putative nongenomic mechanism, which was not interrupted by actinomycin D.