硫化氢对离体大鼠心室肌细胞ATP依赖的钾通道外向电流的影响

目的 观察内源性及外源性硫化氢(hydrogen sulfide,H2S)对大鼠离体心室肌细胞ATP依赖的钾通道(KATP)外向电流的影响,以探讨H2s对心窜肌细胞的作用.方法 对大鼠离体心脏采用胶原酶酶解法得到单个心室肌细胞,采用膜片钳全细胞技术记录DL-propargylglycine(PPG)及不同浓度硫氢化钠(NaHS,外源性H2S的供体)干预前后的KATP什电流.结果 经PPG(200 μmol/L)干预后,KATP峰电流密度(+70 mV)显著减小[干预前后分别为(5.3258±0.7556)pA/pF比(3.7856±0.4312)pA/pF,P＜0.01],且具有时间依赖性.经NaHS(9.375、18.75、37.5、75、150μmoL/L)干预后,KATP峰电流密度呈浓度依赖性增大,至150 μmol/L时峰电流密度明显增大[(6.6310±0.6092)pA/pF比(9.0949±1.0259)pA/pF,P＜0.01].结论 内源性及外源性H2s均可以开放大鼠离体心室肌KATP通道,使KATP电流增加.     

硫化氢对离体大鼠心室肌细胞ATP依赖的钾通道外向电流的影响

Objective To investigate the effects of endogenous and exogenous hydrogen sulfide (H2S) on the KATP current in isolated rat ventricular myoeytes. Methods Ventrieular myoeytes were isolated from rat heart by modified Langendoff perfusion with collagenase. KATP current of single rat ventricular myocytes was recorded by whole-cell patch-clamp technique. Results The density of KATP current was significantly reduced by 200 μmol/L DL-propargylglyeine (PPG, an irreversible inhibitor of the H2S) [(5.3258±0.7556) pA/pF vs. (3.7856±0.4312) pA/pF, P ＜ 0.01] in a time-dependent way. The density of KATP current could be significantly increased by NariS(a H2S donor, 9.375, 18.75, 37.5,75, 150 μmol/L) in a concentration-dependent manner [(6.6310±0.6092) pA/pF vs. (9.0949±1.0259)pA/pF at 150 μmol/L, P ＜ 0.01]. Conclusion Both endogenous and exogenous H2S could open KATP channels and enhance the KATP current in rat ventricular myocytes.     

硫化氢对离体大鼠心室肌细胞ATP依赖的钾通道外向电流的影响

Objective To investigate the effects of endogenous and exogenous hydrogen sulfide (H2S) on the KATP current in isolated rat ventricular myoeytes. Methods Ventrieular myoeytes were isolated from rat heart by modified Langendoff perfusion with collagenase. KATP current of single rat ventricular myocytes was recorded by whole-cell patch-clamp technique. Results The density of KATP current was significantly reduced by 200 μmol/L DL-propargylglyeine (PPG, an irreversible inhibitor of the H2S) [(5.3258±0.7556) pA/pF vs. (3.7856±0.4312) pA/pF, P ＜ 0.01] in a time-dependent way. The density of KATP current could be significantly increased by NariS(a H2S donor, 9.375, 18.75, 37.5,75, 150 μmol/L) in a concentration-dependent manner [(6.6310±0.6092) pA/pF vs. (9.0949±1.0259)pA/pF at 150 μmol/L, P ＜ 0.01]. Conclusion Both endogenous and exogenous H2S could open KATP channels and enhance the KATP current in rat ventricular myocytes.     

硫化氢对离体大鼠心室肌细胞ATP依赖的钾通道外向电流的影响

Objective To investigate the effects of endogenous and exogenous hydrogen sulfide (H2S) on the KATP current in isolated rat ventricular myoeytes. Methods Ventrieular myoeytes were isolated from rat heart by modified Langendoff perfusion with collagenase. KATP current of single rat ventricular myocytes was recorded by whole-cell patch-clamp technique. Results The density of KATP current was significantly reduced by 200 μmol/L DL-propargylglyeine (PPG, an irreversible inhibitor of the H2S) [(5.3258±0.7556) pA/pF vs. (3.7856±0.4312) pA/pF, P ＜ 0.01] in a time-dependent way. The density of KATP current could be significantly increased by NariS(a H2S donor, 9.375, 18.75, 37.5,75, 150 μmol/L) in a concentration-dependent manner [(6.6310±0.6092) pA/pF vs. (9.0949±1.0259)pA/pF at 150 μmol/L, P ＜ 0.01]. Conclusion Both endogenous and exogenous H2S could open KATP channels and enhance the KATP current in rat ventricular myocytes.     

硫化氢对离体大鼠心室肌细胞ATP依赖的钾通道外向电流的影响

Objective To investigate the effects of endogenous and exogenous hydrogen sulfide (H2S) on the KATP current in isolated rat ventricular myoeytes. Methods Ventrieular myoeytes were isolated from rat heart by modified Langendoff perfusion with collagenase. KATP current of single rat ventricular myocytes was recorded by whole-cell patch-clamp technique. Results The density of KATP current was significantly reduced by 200 μmol/L DL-propargylglyeine (PPG, an irreversible inhibitor of the H2S) [(5.3258±0.7556) pA/pF vs. (3.7856±0.4312) pA/pF, P ＜ 0.01] in a time-dependent way. The density of KATP current could be significantly increased by NariS(a H2S donor, 9.375, 18.75, 37.5,75, 150 μmol/L) in a concentration-dependent manner [(6.6310±0.6092) pA/pF vs. (9.0949±1.0259)pA/pF at 150 μmol/L, P ＜ 0.01]. Conclusion Both endogenous and exogenous H2S could open KATP channels and enhance the KATP current in rat ventricular myocytes.     

硫化氢对离体大鼠心室肌细胞ATP依赖的钾通道外向电流的影响

Objective To investigate the effects of endogenous and exogenous hydrogen sulfide (H2S) on the KATP current in isolated rat ventricular myoeytes. Methods Ventrieular myoeytes were isolated from rat heart by modified Langendoff perfusion with collagenase. KATP current of single rat ventricular myocytes was recorded by whole-cell patch-clamp technique. Results The density of KATP current was significantly reduced by 200 μmol/L DL-propargylglyeine (PPG, an irreversible inhibitor of the H2S) [(5.3258±0.7556) pA/pF vs. (3.7856±0.4312) pA/pF, P ＜ 0.01] in a time-dependent way. The density of KATP current could be significantly increased by NariS(a H2S donor, 9.375, 18.75, 37.5,75, 150 μmol/L) in a concentration-dependent manner [(6.6310±0.6092) pA/pF vs. (9.0949±1.0259)pA/pF at 150 μmol/L, P ＜ 0.01]. Conclusion Both endogenous and exogenous H2S could open KATP channels and enhance the KATP current in rat ventricular myocytes.     

硫化氢对离体大鼠心室肌细胞ATP依赖的钾通道外向电流的影响

Objective To investigate the effects of endogenous and exogenous hydrogen sulfide (H2S) on the KATP current in isolated rat ventricular myoeytes. Methods Ventrieular myoeytes were isolated from rat heart by modified Langendoff perfusion with collagenase. KATP current of single rat ventricular myocytes was recorded by whole-cell patch-clamp technique. Results The density of KATP current was significantly reduced by 200 μmol/L DL-propargylglyeine (PPG, an irreversible inhibitor of the H2S) [(5.3258±0.7556) pA/pF vs. (3.7856±0.4312) pA/pF, P ＜ 0.01] in a time-dependent way. The density of KATP current could be significantly increased by NariS(a H2S donor, 9.375, 18.75, 37.5,75, 150 μmol/L) in a concentration-dependent manner [(6.6310±0.6092) pA/pF vs. (9.0949±1.0259)pA/pF at 150 μmol/L, P ＜ 0.01]. Conclusion Both endogenous and exogenous H2S could open KATP channels and enhance the KATP current in rat ventricular myocytes.     

硫化氢对离体大鼠心室肌细胞ATP依赖的钾通道外向电流的影响

Objective To investigate the effects of endogenous and exogenous hydrogen sulfide (H2S) on the KATP current in isolated rat ventricular myoeytes. Methods Ventrieular myoeytes were isolated from rat heart by modified Langendoff perfusion with collagenase. KATP current of single rat ventricular myocytes was recorded by whole-cell patch-clamp technique. Results The density of KATP current was significantly reduced by 200 μmol/L DL-propargylglyeine (PPG, an irreversible inhibitor of the H2S) [(5.3258±0.7556) pA/pF vs. (3.7856±0.4312) pA/pF, P ＜ 0.01] in a time-dependent way. The density of KATP current could be significantly increased by NariS(a H2S donor, 9.375, 18.75, 37.5,75, 150 μmol/L) in a concentration-dependent manner [(6.6310±0.6092) pA/pF vs. (9.0949±1.0259)pA/pF at 150 μmol/L, P ＜ 0.01]. Conclusion Both endogenous and exogenous H2S could open KATP channels and enhance the KATP current in rat ventricular myocytes.     

硫化氢对离体大鼠心室肌细胞ATP依赖的钾通道外向电流的影响

Objective To investigate the effects of endogenous and exogenous hydrogen sulfide (H2S) on the KATP current in isolated rat ventricular myoeytes. Methods Ventrieular myoeytes were isolated from rat heart by modified Langendoff perfusion with collagenase. KATP current of single rat ventricular myocytes was recorded by whole-cell patch-clamp technique. Results The density of KATP current was significantly reduced by 200 μmol/L DL-propargylglyeine (PPG, an irreversible inhibitor of the H2S) [(5.3258±0.7556) pA/pF vs. (3.7856±0.4312) pA/pF, P ＜ 0.01] in a time-dependent way. The density of KATP current could be significantly increased by NariS(a H2S donor, 9.375, 18.75, 37.5,75, 150 μmol/L) in a concentration-dependent manner [(6.6310±0.6092) pA/pF vs. (9.0949±1.0259)pA/pF at 150 μmol/L, P ＜ 0.01]. Conclusion Both endogenous and exogenous H2S could open KATP channels and enhance the KATP current in rat ventricular myocytes.     

硫化氢对离体大鼠心室肌细胞ATP依赖的钾通道外向电流的影响

Objective To investigate the effects of endogenous and exogenous hydrogen sulfide (H2S) on the KATP current in isolated rat ventricular myoeytes. Methods Ventrieular myoeytes were isolated from rat heart by modified Langendoff perfusion with collagenase. KATP current of single rat ventricular myocytes was recorded by whole-cell patch-clamp technique. Results The density of KATP current was significantly reduced by 200 μmol/L DL-propargylglyeine (PPG, an irreversible inhibitor of the H2S) [(5.3258±0.7556) pA/pF vs. (3.7856±0.4312) pA/pF, P ＜ 0.01] in a time-dependent way. The density of KATP current could be significantly increased by NariS(a H2S donor, 9.375, 18.75, 37.5,75, 150 μmol/L) in a concentration-dependent manner [(6.6310±0.6092) pA/pF vs. (9.0949±1.0259)pA/pF at 150 μmol/L, P ＜ 0.01]. Conclusion Both endogenous and exogenous H2S could open KATP channels and enhance the KATP current in rat ventricular myocytes.     

巨噬细胞移动抑制因子对HL-1细胞T型钙电流的调控

目的 观察巨噬细胞移动抑制因子（macrophage migration inhibitory factor,MIF）对心房肌细胞T型钙电流（T-type calcium channel current,ICa,T）的调控.方法 使用全细胞膜片钳和分子生物分析方法检测心房肌细胞ICa,T的表达.结果 在体外培养的心房肌细胞株（HL-1细胞）中,小鼠重组MIF（20、40 nmol/L,24 h）可明显抑制ICa,T的峰值电流,与对照组比较,差异均有统计学意义[峰值内向电流：（-17.5±2.9）pA/pF vs.（-27.9±3.4） pA/pF,P＜0.05;（-11.3±1.7）pA/pF vs.（-27.9±3.4）pA/pF,P＜0.01];并可损伤电压依赖的ICa,T激活,使T型钙通道α1G和α1H亚单位mRNA表达下调.而Src非特异性抑制剂genistein和特异性抑制剂PP1可逆转40 nmol/L MIF所致的ICa,T下调[genistein：（-11.3±1.7）pA/pF vs.（-16.1±0.8）,P＜0.05;PPI：（-11.3±1.7）pA/pFvs.（-19.0±3.2）pA/pF,P＜0.05].结论 MIF可能通过影响ICa,T参与心房颤动的病理过程,Src可能参与该信号转导途径.     

稳心颗粒甘松提取物对大鼠心室肌细胞钠电流和瞬时外向钾电流激活动力学的影响

目的研究步长稳心颗粒中甘松提取物对大鼠心室肌细胞钠电流(INa)、瞬时外向钾电流(Ito)激活动力学的影响。方法采用全细胞膜片钳技术,研究10 g/L甘松提取物对急性分离的成年大鼠心室肌细胞INa、Ito激活动力学的影响。结果①10 g/L甘松提取物使大鼠心室肌细胞INa峰值(INa,max)从-58.96±2.71 pA/pF降至-31.66±1.29 pA/pF(n=5,P<0.01);②10 g/L甘松提取物使Ito峰值(Ito,max)由3.40±1.52 pA/pF降到1.43±0.64 pA/pF(n=7,P<0.05)。10 g/L甘松提取物对INa和Ito的抑制率分别达38.2%和57.9%。结论10 g/L甘松提取物对大鼠心室肌细胞INa、Ito具有显著抑制作用。     

花生四烯酸乙醇胺对乳鼠心肌细胞外向钾通道电流的影响

目的研究内源性大麻样物质花生四烯酸乙醇胺(AEA)对乳鼠心肌细胞瞬时外向钾电流(Ito)及持续外向钾电流(Isus)的作用。方法体外培养乳鼠心室肌细胞,应用全细胞膜片钳方法检测不同浓度的AEA对Ito及Isus的作用。结果20nmol/LAEA即可显著抑制心肌细胞Ito及Isus的电流密度(分别为16.13±3.31pA/pFvs14.48±1.97pA/pF,及11.17±3.25pA/pFvs10.16±3.21pA/pF;P均<0.01)。逐步增加AEA的浓度至100,500nmol/L及1,5,10μmol/L仍然对Ito及Isus有抑制作用,但对Ito电流密度抑制最多的是5μmol/LAEA,而对Isus电流密度产生最大抑制作用的AEA浓度为1μmol/L。结论AEA对体外培养的乳鼠心肌细胞的Ito及Isus具有抑制作用,这一作用在一定的药物浓度范围内随剂量增加而增加。     

卡维地洛对老龄大鼠心房肌细胞起搏电流的作用

目的研究卡维地洛（Car）对大鼠心房肌细胞起搏电流（If）的影响，探讨其降低心房颤动的机制。方法选择22～24月龄SD大鼠分离心房肌细胞，利用全细胞膜片钳技术记录If。结果Car可明显降低老龄大鼠心房肌细胞的超极化激活起搏电流，在-150mV时，1．0μmol／L Car使If的电流密度从（3．2±0．4）pA／pF降至（2．4±0．3）pA／pF（P％0．01）。Car的抑制电流效应呈电压依赖性，即随着超极化电位的增加，Car的效应也增加。在0．1～30．0μmol／L的范围内，Car以浓度依赖性方式阻滞起搏电流，其IC50为1．37μmol／L（95％可信限为1．96～0．57μmol／L）。进一步，Car可以使If的稳态激活曲线向超极化方向移动，使半激活电压从（-87．5±2．3）mV移至（-96．2±4．7）mV。从而使电流激活减慢，这可能是其减少，If的主要原因。结论卡维地洛可明显降低老龄大鼠心房肌细胞起搏电流密度。     

心房颤动24h和48h对犬心房肌有效不应期及L型钙电流的影响

目的 研究犬心房颤动（房颤）持续24h和48 h,心房肌有效不应期和L型钙电流变化的一致性及其机制.方法 健康成年杂种犬18只,分为对照组、24 h房颤组、48 h房颤组,每组6只.600次/min起搏高右心房建立犬房颤模型,应用程序刺激的方法测定右心房有效不应期（ERP）,通过Langendorff左回旋支灌流分离心房肌细胞,并通过全细胞膜片钳技术记录L型钙电流（ICa-L）变化.应用免疫组织化学方法检测各组心房组织L型电压依赖性钙通道（LVDCC）α1c蛋白表达.用图像分析系统对组织化学抗原表达进行半定量分析.结果 所有实验动物均可诱发出房颤.心房ERP的变化在最初6h较对照组明显缩短,后直至48 h呈进行性缩短.快速起搏6h后ERP（129.50±8.64）ms较对照组（141.00±15.23）ms缩短（12.13±2.24）ms（P＜0.01）,24 h后心房ERP（123.00± 13.37） ms缩短（19.23±2.14）ms（P＜0.01）,48 h缩短（28.15±4.26）ms（P＜0.01）.同时在房颤持续过程中24h房颤可引起ICa-L电流密度（-4.83±0.30）pA/pF较对照组（-6.69±0.08）pA/pF减小,48 h（-3.70±0.50）pA/pF减少的程度更重.24 h房颤及48 h房颤犬的左、右心房组织LVDCC α1c蛋白表达均较对照组明显减少（P＜0.05）,48 h房颤组减少程度更重（P＜0.01）.结论 房颤持续24 h,心房肌ERP显著缩短、ICa-L密度降低.房颤持续48 h仍然维持L型钙通道改变特征.提示：钙通道阻断剂可用于持续24 h房颤,预防房颤复发.     

山莨菪碱对兔缺血再灌注后心室肌细胞L-钙离子通道电流的影响

目的研究山莨菪碱对兔在体缺血再灌注后心室肌细胞L-钙离子通道电流的影响,探讨山莨菪碱抗再灌注心律失常的细胞学离子机制。方法 45只新西兰大耳白兔按随机数字表法随机分为3组:缺血再灌注动物模型组(I-R组,结扎冠状动脉左前降支30min后再开放120min);山莨菪碱治疗组(Ani组,手术前1min给予动物耳缘静脉注射山莨菪碱5mg/kg);假手术对照组(只开胸不结扎血管)。采用酶解的方法分离缺血部位心室肌外膜单个心室肌细胞,应用全细胞膜片钳技术记录L-钙离子通道电流。结果 (1)I-R组、Ani组室性心动过速和心室颤动发生率均比对照组高,差异有统计学意义(P0.05);Ani组室性心动过速和心室颤动发生率明显低于I-R组,差异有统计学意义(26.7%(4/15)vs.40%(6/15),P0.05;6.7%(1/15)vs.26.7%(4/15),P0.05)。与对照组比较,I-R组心律失常评分升高,差异有统计学意义[(3.6±0.8)分vs.(1.1±0.3)分,P0.01];Ani组心律失常评分差异无统计学意义[(2.6±0.7)分vs.(1.1±0.3)分,P0.05]。(2)I-R组电流密度峰值(0mV)较对照组显著升高,差异有统计学意义[(-4.34±0.92)pA/pFvs.(-3.13±1.22)pA/pF,P0.05];Ani组电流密度峰值较I-R组明显下降,差异有统计学意义[(-3.25±0.79)pA/pFvs.(-4.34±0.92)pA/pF,P0.05]。Ani组电流密度峰值与对照组比较,差异无统计学意义[(-3.25±0.79)pA/pFvs.(-3.13±1.22)pA/pF,P0.05]。结论山莨菪碱可逆转缺血再灌注心室肌细胞的电重构,这可能是其降低心律失常发生率的细胞学离子机制。     

丹酚酸B对大鼠心室肌细胞瞬时外向钾电流和L型钙电流的阻滞作用

目的研究从丹参中分离提取的药物单体——丹酚酸B对大鼠心肌细胞上的瞬时外向钾电流(Ito)、内向整流钾电流(IK1)和L型钙电流(ICa,L)的电生理学作用。方法用酶解法分离大鼠心室肌细胞,全细胞膜片钳技术记录Ito、IK1和ICa,L。每个细胞采用加药前后自身对照,用含100μmol/L丹酚酸B的细胞外液灌流心室肌细胞,记录加药前、后的电流,所有数据均在细胞破膜后20min内完成。结果 100μmol/L的丹酚酸B对Ito和ICa,L具有抑制作用,使Ito和ICa,L最大激活峰值电流密度下降,电流密度-电压曲线下移;且丹酚酸B主要抑制Ito的快速电流成分Itof,而对Ito的缓慢电流成分Itos无明显作用。在60mV测试电压下,Itof的最大激活峰值电流密度从23.51±3.29pA/pF降为16.85±2.36pA/pF,抑制率为28.31%±10.6%(n=8,P0.05)。在-10mV测试电压下,100μmol/L丹酚酸B作用后ICa,L的最大激活峰值电流密度从-8.66±-2.40pA/pF降为-5.91±-2.14pA/pF,抑制率为31.84%±10.23%(n=11,P0.05)。丹酚酸B使Ito通道失活后的恢复减慢,但不改变ICa,L的通道动力学。丹酚酸B对IK1无显著作用。结论丹酚酸B对Ito和ICa,L具有阻滞作用,而对IK1无显著作用。     

罗格列酮对四氧嘧啶介导的糖尿病家兔心室肌细胞L型钙通道电流的影响

目的探讨罗格列酮对家兔心室肌细胞L型钙通道电流(I_(CaL))的影响。方法四氧嘧啶建立糖尿病家兔模型后,利用酶解法急性分离心室肌细胞,用全细胞膜片钳技术观测糖尿病和罗格列酮对心肌细胞I_(CaL)的影响,并与正常家兔进行比较。结果 (1)正常组家兔心室肌细胞I_(CaL)电流密度[(-8.83±2.31)pA/pF]大于糖尿病组[(-8.84±1.98)pA/pF],但差异不具有统计学意义。(2)给予罗格列酮后正常和糖尿病家兔组心室肌细胞I_(CaL)[正常组:基线电流密度(-8.83±2.31 pA/pF)大于5 min电流密度(-4.17±1.89 pA/pF)和10 min电流密度(-5.54±1.63)pA/pF,糖尿病组:基线电流密度(-8.84±1.98)pA/pF大于5 ml‘n电流密度(-4.97±1.15)pA/pF和10 min电流密度(-3.89±1.06)pA/pF],各时段差异均有统计学意义(各组P<0.05)。(3)空腹血糖[(7.65±1.60)mmol/L]小于建模48 h[(17.72±9.15)mmol/L]及1周后空腹血糖[(20.84±9.48)mmol/L]。各时段胰岛素水平[空腹(23.45±9.22)mmol/L,48 h后(22.69±8.94)mmol/L,1周后(21.65±11.91)mmol/L]差异均无统计学意义(各组P>0.05)。结论正常家兔组I_(CaL)电流密度与糖尿病家兔组相似,提示糖尿病对心肌细胞I_(CaL)无明显影响;罗格列酮对心脏的作用不依赖于高血糖存在与否,提示罗格列酮可能通过某些与胰岛素水平有关的特定机制作用于心肌细胞;四氧嘧啶所致糖尿病模型是一种不完全等同于1型及2型糖尿病的独特模型,但去除了胰岛素抵抗的影响。该模型可以用来作为高血糖对心肌细胞离子通道影响的研究载体。     

雌激素对高血压人体肠系膜动脉平滑肌细胞大电导钙激活钾通道的作用研究

目的 研究雌激素（E）对非高血压（NH）及原发性高血压（EH）人体肠系膜动脉平滑肌细胞（HMASMC）大电导钙激活钾通道（BKCa channels）及自发性瞬时外向电流（STOCs）的作用,探讨雌激素在NH及EH下对该通道作用的差异性.方法 急性酶分离法分离获取单个HMASMC,采用全细胞穿孔膜片钳技术记录该细胞上的BKCa和STOCs.结果 雌激素可明显激活NH组HMASMC上的BKCa和STOCs,在测试电压范围内,雌激素使膜电位从0到＋60 mV时BKCa的电流密度均显著性增加,在0和＋60 mV时其电流密度分别从（1.95±0.39）pA/pF、（15.40±4.27）pA/pF增加到（2.81±0.84）pA/pF（P＜0.05,25例）、（26.55±6.24）pA/pF（P＜0.01,25例）,其中0 mV时增加了0.44倍,＋60 mV时增加了0.72倍;电位为-20 mV时STOCs的幅度和频率分别从（7.920±2.031）pA、（3.15±0.79）Hz增加到（12.92±3.41）pA（P＜0.05,25例）、（4.41±0.96）Hz（P＜0.01,25例）,其中幅度增加了0.63倍,频率增加了0.40倍.而EH组在测试的-60到＋50 mV电压范围,雌激素没有这种显著性激活作用,在0和＋60 mV时其电流密度分别从（1.34±0.43）pA/pF、（4.91±1.40）pA/pF增加到（1.53±0.55）pA/pF（P＞0.05,14例）、（8.04±2.0）pA/pF（P＜0.05,14例）,其中0 mV时增加了0.14倍,＋60 mV时增加了0.63倍;在电位为-20 mV时STOCs的幅度和频率分别从（5.39±1.93）pA、（0.75±0.37）Hz增加到（6.70±1.06）pA（P＞0.05,14例）、（2.34±0.98）Hz（P＜0.05,14例）,其中幅度增加了0.24倍,频率增加了2.12倍.结论 雌激素对NH组HMASMC上的BKCa和STOCs有明显的激活作用,而在EH组这种激活作用显著降低,由此推测EH组HMASMC对雌激素的反应性较NH组低,这种差异性将为雌激素合理应用于临床提供有力的实验依据. 关键词：高血压;雌激素;人体肠系膜动脉;平滑肌细胞;自发性瞬时外向电流;大电导钙激活钾通道