血管紧张素Ⅱ及替米沙坦对大鼠心房肌细胞钾和钙电流的影响

目的研究血管紧张素Ⅱ(AngⅡ)和替米沙坦对SD大鼠心房肌细胞瞬时外向钾电流(Ito)和L型钙电流(ICa-L)的作用。方法急性酶解法分离SD大鼠心房肌细胞,采用全细胞膜片钳技术,观察AngⅡ、替米沙坦以及AngⅡ联合替米沙坦对大鼠心房肌细胞Ito和ICa-L的影响。结果 AngⅡ(0.1μmol/L)和替米沙坦(0.01μmol/L)以及两药联合均能抑制大鼠心房肌细胞Ito,AngⅡ组、替米沙坦组、联合组干预前后Ito的电流密度值比较差异有统计学意义[(22.48±2.75)vs(15.71±2.06)pA/pF,(24.16±2.36)vs(16.15±1.82)pA/pF,(24.41±2.27)vs(21.35±1.46)pA/pF,P<0.05]。AngⅡ(0.1μmol/L)能显著增强大鼠心房肌细胞ICa-L的峰值电流密度[(-4.51±0.38)vs(-5.16±0.29)pA/pF,P<0.01];替米沙坦(0.01μmol/L)对心房肌细胞ICa-L无明显作用[(-4.35±0.27)vs(-4.29±0.34)pA/pF,P>0.05],但联合组中替米沙坦可拮抗AngⅡ对ICa-L的增强效...     

AngⅡ对人心房肌细胞膜钾通道电流的影响及替米沙坦的拮抗作用

目的: 观察AngⅡ对人心房肌细胞膜钾电流的作用,揭示其参与房性心律失常的电生理机制,为应用AngⅡ受体拮抗剂治疗房性心律失常提供实验基础.方法: 急性分离单个人心房肌细胞,采用全细胞膜片钳方法记录内向整流钾电流(Ik1)、短暂外向钾电流(Ito).实验分4组:对照组,AngⅡ(0.1 μmol/L)组,替米沙坦(0.01 μmol/L)组,AngⅡ 替米沙坦组.结果: 与对照组相比,0.1 μmol/L AngⅡ使人心房肌细胞膜Ito峰值电流密度明显下降(pA/pF, 6.55±0.52 vs 12.65±1.06,P＜0.01), 在-100mV电压下使IK1 峰值电流密度显著升高 (pA/pF, -9.31±1.02 vs -5.23±0.98, P<0.01).0.01 μmol/L替米沙坦对人心房肌细胞膜Ito IK1无明显影响,但可拮抗AngII的作用;AngⅡ 替米沙坦组的Ito峰值电流密度 (pA/pF,11.74±1.28 )和IK1 峰值电流密度(pA/pF, -6.13±1.15) 与AngⅡ组相比有显著差别(P＜0.01).结论: AngⅡ对人心房肌细胞具有明显的电生理学作用,0.1 μmol/L AngⅡ可促进人心房肌细胞膜IK1并抑制Ito,替米沙坦可拮抗AngⅡ对人心房肌细胞膜钾电流的作用.     

淫羊藿苷对兔心室肌细胞L-型钙电流的影响

目的:利用膜片钳技术研究淫羊藿苷(ICA)对兔单个心室肌细胞L-型钙电流(ICa,L)的影响。方法:采用酶解法分离兔单个心室肌细胞,应用全细胞膜片钳技术观察10,20,40μmol/L的ICA对心室肌细胞ICa,L的作用。结果:①10,20,40μmol/L的ICA使兔心室肌细胞ICa,L最大峰电流密度从(15.81±1.23)pA/pF分别降至(11.27±0.89)pA/pF,(9.48±0.85)pA/pF和(6.87±0.81)pA/pF(n=6,P<0.05),抑制率分别为28.7%,40.0%和56.5%;ICA使ICa,L的电流-电压曲线上移,但不改变其基本形状;②20μmol/L ICA可以使钙通道稳态失活曲线左移并可减慢L-型钙通道失活后的恢复过程。结论:ICA对ICa,L具有浓度依赖性阻滞作用,这可能是其抗心律失常的重要机制之一。     

槲寄生黄酮苷对大鼠心室肌细胞钾离子通道的作用

目的观察槲寄生黄酮苷对大鼠心室肌细胞钾离子通道的作用,探讨槲寄生黄酮苷抗心律失常作用机制。方法应用全细胞膜片钳技术记录槲寄生黄酮苷对大鼠单个心室肌细胞内向整流钾电流(IK1)、瞬时外向钾电流(Ito)的影响。结果应用50μg/ml和250μg/ml两种浓度的槲寄生黄酮苷分别使大鼠单个心室肌细胞内向整流钾电流(IK1)在实验电压-120mV时从给药前(-26.23±9.52)pA/pF减少到(-20.82±7.88)pA/pF,(-18.11±7.89)pA/pF(n=7,P<0.05);使大鼠心室肌细胞瞬时外向钾电流(Ito)在实验电压+50mV时,从给药前(26.14±6.67)pA/pF减少到(16.41±6.23)pA/pF,(13.25±3.78)pA/pF(n=4,P<0.05)。结论槲寄生黄酮苷抑制大鼠心室肌细胞IK1,Ito可能是其抗心律失常作用的一个机制。     

过氧化氢对大鼠心室肌细胞钠通道电流的影响

目的 研究过氧化氢(H2O2)对单个大鼠心室肌细胞钠通道电流(INa)的影响.方法 用急性酶解法获得单个大鼠心室肌细胞;用标准的全细胞膜片钳技术记录钠通道电流,观察1 mmol/L H2O2引起单个大鼠心室肌细胞INa改变.结果 在1 mmol/L H2O2作用下,大鼠心室肌细胞INa峰值电流密度从(19.95±4.58)pA/pF减少至(15.19±4.15)pA/pF(n=8,P＜0.05),电流-电压曲线上移,翻转电位左移,但对激活电位、峰电位无明显影响;H2O2对INa稳态激活曲线无明显改变,V0 5从(-64.54±0.16)mV左移至(-66.28±0.32)mV(n=8,P＞0.05),对其稳态失活曲线无明显改变,V0 5从(-91.46±0.17)mV左移至(-94.52±0.25)mV(n=8,P＞0.05);H2O2对INa失活后再激活曲线有明显改变,对照组τ为(6.43±1.04)ms,H2O2组τ为(8.31±1.48)ms(n=6,P＜0.05).结论 过氧化氢可以减少大鼠心肌细胞INa,且使其复活明显减慢.     

高浓度姜黄素对大鼠心室肌细胞瞬时外向钾电流和内向整流钾电流的影响

目的研究高浓度姜黄素对大鼠心室肌细胞瞬时外向钾电流(Ito)和内向整流钾电流(Ik1)的影响。方法采用急性酶解分离法获得大鼠心室肌细胞,以全细胞膜片钳技术记录Ito和Ik1,观察50μmol/L姜黄素对Ito和Ik1的影响。结果 50μm/L姜黄素对Ito和Ik1通道电流的抑制率分别是(84±11)%(P<0.05)和(59±8)%(P<0.01)。它使Ito和Ik1通道电流密度-电压曲线电流幅度减小,但不改变其整流特性。结论 50μmol/L姜黄素能明显抑制大鼠心室肌细胞Ito和Ik1电流,提示其可能存在心脏毒性作用。     

参松养心胶囊对心室肌细胞钾通道的影响

目的观察参松养心胶囊干粉提取溶液对大鼠单个心室肌细胞内向整流钾电流(IK1)、瞬时外向钾电流(Ito)以及豚鼠心肌细胞延迟整流钾电流(Ik)的影响。方法用酶解法分离单个心室肌细胞,并用全细胞膜片钳记录技术。结果当药物浓度0.5%时,可以使大鼠心肌细胞IK1内向成分降低,使-100mV时IK1电流密度从(-10.8±1.8)pA/pF降至(-7.2±2.1)pA/pF,平均抑制率为(33.1±16.9)%(n=11,P<0.05),但不改变电流的翻转电位及整流特性。药物同时对Ito电流的瞬时成分有抑制作用,60mV时Ito电流密度从(-19.8±7.1)pA/pF降至(-10.0±3.9)pA/pF,平均抑制率为(50.6±10.8)%(n=6,P<0.05),稳态失活曲线左移,失活后恢复时间常数增大。药物浓度0.5%时,对Ik有电压依赖性抑制作用,50mV时对尾电流峰值的抑制率为(30.8±1.1)%(n=5,P<0.05)。结论参松养心胶囊干粉提取溶液对IK1,Ito和Ik均具有不同程度的阻滞作用。这种多离子通道阻滞作用不仅使参松养心胶囊具有广谱的抗心律失常疗效,减少致心律失常的副作用,对Ito的阻滞效应还将显示其独特的抑制2相折返的作用,值得对其作更深入和广泛的研究。     

BRL-37344对豚鼠心肌细胞ICa-L、Ito的影响

目的 为研究β3肾上腺素能受体介导的心脏生物学效应--β3肾上腺素能受体激活后心肌细胞电生理活动的变化.方法 以原代培养的豚鼠心肌细胞为对象, 采用全细胞膜片钳技术记录心肌细胞孵育β3肾上腺素能受体激动剂4-[-[2-hydroxy-(3-chlorophenyl)ethyl-amino]propyl]phenoxyacetate(BRL-37344; BRL)5~10 min前后ICa-L,Ito(L型钙离子通道和瞬时外向钾通道)的变化.结果 显示10-6 mol/L的BRL显著增强豚鼠心肌细胞的Ito,上移I-V曲线;去极化刺激到+80 mV时,电流密度从(6.11±1.03) pA/pF上升到(8.46±2.07) pA/pF(n=6,P=0.013064).10-6 mol/L的BRL显著增强豚鼠心肌细胞的ICa-L,为对照组的(2.30±0.75)倍(n=5,P=0.0063);去极化刺激到+10 mV时,电流幅度从(89.25±17.83) pA上升到(205.00±72.24) pA.结论 BRL-37344可增强豚鼠心肌瞬时外向钾电流和L型钙电流,进而调控心脏的活动.     

哇巴因诱发大鼠心律失常作用靶点的研究

目的　观察哇巴因对大鼠心室肌细胞动作电位时程、钾通道的作用 ,探讨哇巴因诱发心律失常的作用机制 ,为寻找新的抗心律失常药物提供依据。方法　应用全细胞膜片钳技术记录哇巴因对大鼠心肌细胞动作电位时程 (APD)、内向整流钾电流 (Ik1 )、瞬时外向钾电流 (Ito)的作用。结果　①哇巴因 5μmol/L使大鼠心室肌细胞动作电位时程从给药前的 86 .3ms± 2 5 .2ms(APD90 ) ,缩短至 58.9ms± 2 0 .8ms(n =5 ,P <0 .0 1 ,给药 1 0min) ;②哇巴因 5μmol/L可增加大鼠心室肌细胞内向整流钾电流 ,使Ik1 从 - 1 868pA± 1 88pA增加到 - 2 393pA± 367pA(刺激电压 - 1 2 0mV ,n=1 0 ,P <0 .0 1 ) ;③哇巴因 5μmol/L可增加大鼠心室肌细胞瞬时外向钾电流 ,使Ito从 1 2 73pA± 31 8pA增加到 1 70 7pA± 486pA(刺激电压 +60mV ,n =5 ,P <0 .0 1 )。结论　哇巴因诱发室性心律失常可能与它缩短心室肌细胞动作电位时程有关 ,而Ito的增加使二期平台期缩短 ,Ik1 的增加使三期复极加快 ,均参与了动作电位时程缩短的过程。同时增加Ik1 将影响静息膜电位 ,可能使膜反应性增强     

卡维地洛对大鼠心室肌细胞Ito电流影响的实验研究

目的探讨卡维地洛对大鼠心室肌细胞瞬时外向钾电流(Ito)的作用.方法采用胶原酶酶解法分离得到大鼠单心室肌细胞;采用膜片钳全细胞技术记录灌流卡维地洛前后Ito电流的变化.结果灌流0.1 mM及1.0 mM卡维地洛后,Ito电流密度分别为(pA/pF)(5.06±1.98),(3.91±0.66),P＜0.05;不同去极化电压水平Ito电流值也有明显减小,Ⅰ-Ⅴ曲线向下方移位.结论卡维地洛对大鼠心室肌细胞Ito电流具有抑制作用,此抑制作用呈浓度依赖趋势.     

CPUHY002对大鼠心肌细胞瞬时外向钾电流的影响

目的观察一种新合成的磷酸二酯酶Ⅲ(PDEⅢ)抑制剂CPUHY002对大鼠心肌细胞瞬时外向钾电流(Ito)的影响。方法采用全细胞膜片钳技术考察CPUHY002对急性分离大鼠心肌细胞和H9c2细胞系Ito的作用。结果在+50 mV下,CPUHY002对急性分离细胞和H9c2细胞系的Ito呈浓度依赖性抑制,其半数有效抑制浓度(IC50)分别为0.98μmol/L和0.91μmol/L;1μmol/L CPUHY002可使I-V曲线明显下移,Ito峰值分别下降(39.10±2.30)%和(47.32±2.06)%,激活曲线右移,失活曲线左移(未见于H9c2),恢复曲线无显著变化。结论 CPUHY002可浓度依赖性地抑制大鼠心肌细胞Ito。     

肾上腺髓质素对脓毒性休克大鼠心肌细胞外向钾电流的影响

目的 研究肾上腺髓质素(ADM)对脓毒性休克大鼠心肌细胞外向钾电流的影响.方法 成年大鼠腹腔注射脂多糖(LPS,10 mg/kg)4 h后,分离心室肌细胞.用全细胞膜片钳的方法 记录瞬时外向钾电流(I_(to)),稳态钾电流(I_(ss))和ATP敏感钾电流(I_(K,ATP)).结果 LPS处理对I_(to)和I_(ss)无影响.休克心肌细胞I_(K,ATP)密度[(2.66 ± 0.56)pA/pF(n=12)]较正常心肌细胞值[(0.27 ± 0.08)pA/pF(n=14)]明显增加(P＜0.01).ADM受体拮抗剂ADM-(22-52)可使增加的I_(K,ATP)得到明显的恢复[(0.69 ± 0.21)pA/pF(n=11),P＜0.01 vs LPS 组].而ADM-(22-52)与100 μmol/L氨基胍联合处理几乎可完全取消I_(K,ATP)的增加.结论 脓毒性休克大鼠心肌细胞I_(K,ATP)被激活.ADM 与NO共同参与了脓毒性休克大鼠心肌细胞I_(K,ATP)的激活.     

兔心肌梗死后右心室肌细胞离子通道电流的变化

目的探讨心肌梗死后右心室肌细胞离子通道电流的变化.方法该研究采用结扎兔冠状动脉左前降支的方法建立心肌梗死动物模型,应用膜片钳全细胞记录方法,记录心肌梗死后2个月右心室心肌细胞钠通道电流(INa)、L-钙通道电流(ICa-L)、瞬间外向钾电流(Ico)的变化.结果心肌梗死后2个月,心肌梗死组INa电流密度峰值[(20.42±1 73)pA/pF,n=15]较对照组[(35 40±3.43)pA/pF,n=16]明显下降(P＜0.05);心肌梗死组ICa-L电流密度峰值[(5.71±0.93)pA/pF,n=12]与对照组[(6.28±1.03)pA/pF,n=10]略下降,但无明显差异(P＞0.05);心肌梗死组Ito电流密度( 60 nV时)[(8.61±0.95)pA/pF,n=16]较对照组[(14.38±1.24)pA/pF,n=17]明显下降(P＜0.05).结论心肌梗死可引起右心室肌细胞INa和Ito的下降,造成心肌传导速度下降和动作电位时程相对延长、复极异常,可能是导致心肌梗死后出现室性心律失常的离子机制.     

Electrical remodeling of membrane ionic channels of hypertrophied ventricular myocytes from spontaneously hypertensive rats

Ｍｅｔｈｏｄｓ　Ｍｅｍｂｒａｎｅｉｏｎｉｃｃｈａｎｎｅｌｓｗｅｒｅｓｔｕｄｉｅｄｉｎｅｎｚｙｍａｔｉｃａｌｌｙｄｉｓｐｅｒｓｅｄｓｐｏｎｔａｎｅｏｕｓｌｙｈｙｐｅｒｔｅｎｓｉｖｅｒａｔｓ (ＳＨＲｓ)ｌｅｆｔｖｅｎｔｒｉｃｕｌａｒｍｙｏｃｙｔｅｓｕｓｉｎｇｔｈｅｗｈｏｌｅ ｃｅｌｌｃｏｎｆｉｇｕｒａｔｉｏｎｏｆｐａｔｃｈ ｃｌａｍｐｔｅｃｈｎｉｑｕｅ ,ｗｉｔｈｎｏｒｍａｌＷｉｓｔａｒｒａｔｓｖｅｎｔｒｉｃｕｌａｒｍｙｏｃｙｔｅｓａｓｃｏｎｔｒｏｌｓ Ｗｅｏｂｓｅｒｖｅｄｄｅｐｏｌａｒｉｚｉｎｇｃｕｒｒ…     

银杏叶提取物对家兔心室肌细胞瞬时外向钾电流和动作电位的影响

目的:探讨银杏叶提取物(Egb761)对家兔心室肌细胞瞬时外向钾电流(Ito)和动作电位的作用,揭示其抗心肌缺血及缺血引起的心律失常的离子机制。方法:酶解法分离家兔的心室肌细胞。全细胞膜片钳技术记录心肌细胞的Ito和动作电位及其被Egb761作用后的变化。结果:①在电压钳制方式下,60μg/L Egb761作用心室肌细胞5 min后,各个钳制电位下的Ito均明显增大,在钳制电位为+50 mV时,Egb761使Ito的电流密度由对照组的(7.59±0.19)pA/pF增加到(11.18±0.89)pA/pF(P<0.01,n=8),Egb761还使Ito的I-V曲线比对照组Ito的I-V明显抬高,但I-V曲线方向没有发生改变,表明Egb761引起了心肌细胞Ito的明显外流。②在电流钳制下,对照组心室肌细胞动作电位都具有从0期到4期的动作电位形态,60μg/L Egb761使心肌细胞动作电位形态呈三角形尖锥锋形,动作电位时程(APD)明显缩短,其复极化50%时程(APD50)和复极化90%时程(APD90)分别由(83.6±4.3)ms缩短为(51.3±3.2)ms和由(168.7±4.1)ms缩短为(93.8±4.4)ms(分别与对照组相比,P<0.01,n=8),尽管Egb761使动作电位幅度(APA)和静息电位(RP)降低,但与对照组相比,没有显著性差异(P>0.05)。结论:Egb761可使心室肌细胞Ito显著增加和APD明显缩短,从而减轻心肌缺血时细胞内阳离子超载对心肌造成的损伤和心肌缺血引起的心律失常的发生,以及增加心脏泵血功能。     

The effects of paeoniflorin monomer of a Chinese herb on cardiac ion channels

Background  Because of the potential proarrhythmic effect of current antiarrhythmic drugs, it is still desirable to find safer antiarrhythmic drugs worldwide. Paeoniflorin is one of the Chinese herb monomers that have different effects on many ion channels. The present study aimed to determine the effects of paeoniflorin on cardiac ion channels.

Methods  Whole-cell patch-clamp technique was used to record ion channel currents. L-type calcium current (I_Ca-L), inward rectifier potassium current (I_K1), and transient outward potassium current (I_to1) were studied in rat ventricular myocytes and sodium current (I_Na), slow delayed rectifier current (I_Ks), and HERG current (I_Kr) were investigated in transfected human embryonic kidney 293 cells.

Results  One hundred μmol/L paeoniflorin reduced the peak I_Ca-L by 40.29% at the test potential of +10 mV (from (–9.78±0.52) pA/pF to (–5.84±0.89) pA/pF, n=5, P=0.028). The steady-state activation curve was shifted to more positive potential in the presence of the drug. The half activation potentials were (–11.22±0.27) mV vs. (–5.95±0.84) mV (n=5, P=0.007), respectively. However, the steady-state inactivation and the time course of recovery from inactivation were not changed. One hundred μmol/L paeoniflorin completely inhibited the peak I_Na and the effect was reversible. Moreover, paeoniflorin inhibited the I_K1 by 30.13% at the test potential of –100 mV (from (–25.26±8.21) pA/pF to (–17.65±6.52) pA/pF, n=6, P=0.015) without effects on the reversal potential and the rectification property. By contrast, 100 μmol/L paeoniflorin had no effects on I_to1, I_Ks or I_Kr channels.

Conclusions  The study demonstrated that paeoniflorin blocked I_Ca-L, I_Na, and I_K1 without affecting I_to1, I_Ks, or I_Kr. The multi-channel block effect may account for its antiarrhythmic effects with less proarrhythmic potential.

     

Verapamil modulating arsenic trioxide-induced QT interval rolongation in guinea pig

Objective To investigate therapeutic action of verapamil on QT prolongation induced by arsenic trioxide (As2O3) in guinea pig and to further explore its possible mechanism. Methods Different doses of As2 O3 was infused intravenously to observe the changes of QT interval on the electrocardiogram (ECG) at different times in guinea pig. Patchclamp technique and laser scanning confocal microscopy were utilized to study the action of As2 O3 on action potential duration (APD),L-type calcium current (ICa-L ), rapid delayed rectifier potassium current (IKr) and intracellular calcium concentration ([Ca2+]i) of guinea pig myocytes. At the same time, verapamil was applied preliminarily to evaluate effects of verapamil on changes of the above index induced by As2O3. Results Intravenous administration of As2 O3 at the dose of 1.6mg/kg and 0.8mg/kg prolonged QT interval on ECG obviously in guinea pig hearts dose dependently and time dependently. QTc (corrected QT interval) was progressively prolonged in the 2-hour period of intravenous infusion of 1.6mg/kg As2O3 from (328.5 ± 30.9)ms of control to (388.4 ± 31.3)ms at 2h following As2O3 ( P ＜ 0.01) .When verapamil was pretreated for 5min, then 1.6mg/kg As2 O3 was added, the results showed that QTe was shorter in verapamil-treatment group (357.3±21.4)ms than that in As2O3 group (388.4±31.3)ms (P＜0.05) at 2h. Confocal experiments showed that in normal Tyrode solution, As2 O3 (1μmol/L and 10μmol/L) had no obvious effects on resting [Ca2+]i (P＞0.05) in guinea pig cardiomyocytes, however, 10μmol/L As2 O3 could markedly enhance [Ca2+]i increase induced by KCl 60mmol/L and the peak value increased from 903.4±369.4 to 1674.6±563.2 ( P＜0.05). The action of elevating [Ca2+]icould be blocked by 10μmol/L verapamil incompletely. The patch-clamp studies indicated that As2 O3 at concentration of 10μmol/L prolonged APD50 from (263.6 -±75.2)ms to (523.9±47.8)ms (P＜0.01) and APD90 from (277.5 ± 77.5)ms to (536.3 ±49.6)ms (P ＜0.01) ,and increased ICa-L from (- 6.0±1.5)pA/pF to (-8.7±2.0)pA/pF (P＜0.01) at 0mV and also reduced IKr from (6.7±1.8)pA/pF to (4.5±1.8)pA/pF (P＜0.05). However, 10μmol/L verapamil could modulate prolonging APD50 from (523.9 ± 47.8) ms to (340.4±83.8) ms ( P＜0.01) and APD90 from (536.3 ±49.6)ms to (348.9 ± 85.5)ms (P＜0.01) and correct increasing Ica-L induced by 10μmol/L As2O3 from (-8.7±2.0)pA/pF to ( - 6.6±1.4)pA/pF (P＜0.05) at 0mV. Conclusion As2O3 could induce prolongation of the QT interval on the ECG in guinea pig hearts and the ionic mechanism is associated with increasing Ica-L and inhibiting IKr/HERG. Verapamil may be useful in normalizing QT prolongation during As2 O3 therapy by decreasing Ica-L and [Ca2+]iof ventricular myocytes in guinea pig.     

Verapamil modulating arsenic trioxide-induced QT interval prolongation in guinea pig

Objective To investigate therapeutic action of verapamil on QT prolongation induced by arsenic trioxide （As2O3） in guinea pig and to further explore its possible mechanism. Methods Different doses of As2O3 was infused intravenously to observe the changes of QT interval on the electrocardiogram （ECG） at different times in guinea pig. Patchclamp technique and laser scanning confocal microscopy were utilized to study the action of As2O3 on action potential duration （APD）,     

Long-term effects of imidapril on calcium and potassium currents in rabbit left ventricular hypertrophic myocytes

Cardiachypertrophy ,inducedby pressureoverload ,isassociatedwithalterationsintheelectrophysiologicpropertiesoftheheart,whichmaycontributetotheincreasedincidenceofventriculararrhythmias 1,2 Amongmanyfactorsinducinghearthypertrophy ,therenin angiotensinsystem (RAS) playsanimportantroleintheregulationofcardiaccellsandmatrixgrowth AngiotensinⅡlevelcanbepartiallyreducedafteradministrationofangiotensinconvertingenzyme (ACE)inhibitors ACEinhibitorshavebeenshowntodecreaseventricularhypertrophyandr…