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1、—1050—重庆医科大学学报2008年第33卷第9期(JournalofChongqingMedicalUniversity2008.Vol.33No.9)论著文章编号:0253-3626(2008)09-1050-04压力超负荷左室肥厚大鼠心肌组织血管紧张素Ⅱ受体的表达王玉兵12,陈明(1.四川省南充市川北医学院附属医院心内科,南充637000;2.重庆医科大学附属第一医院心内科,重庆400016)【摘要】目的:本研究观察压力超负荷左室肥厚(Leftventricularhypertrophy,LVH)大鼠心肌组织AT1和AT2的表达,进一步探讨血管紧张素Ⅱ(Angiotens
2、inⅡ,AngⅡ)受体在左室肥厚中的作用及可能机制。方法:采用腹主动脉缩窄法建立LVH模型,14只Sprague-Dawley(SD)大鼠随机分为:(1)假手术组(n=7);(2)手术组(手术组n=7);用免疫组化法及RT-PCR检测血管紧张素Ⅱ受体(AT)的表达,同时检测LVH的指标:心肌纤维化、左室质量指数(LVMI)、心肌细胞横切面积(CSA)、心肌细胞凋亡指数。结果:与假手术组比较,手术组SBP、DBP、MBP、LVMI、心肌细胞CSA、心肌细胞凋亡指数(Apoptosisindex,APOI)、血浆AngⅡ水平及AT1和AT2蛋白和mRNA的表达水平均显著升高。结论:左
3、室肥厚大鼠心肌组织AT1和AT2从蛋白和mRNA表达水平均明显升高;AT1和AT2均参与左室肥厚过程,但二者可能发挥相互拮抗的作用。【关键词】左室肥厚;血管紧张素Ⅱ;受体【中国图书分类法分类号】R541.3【文献标识码】A【收稿日期】2007-12-03ExpressionofcaraiomyocyteangiotensinⅡreceptorsinratwithpressureoverload-inducedleftventricularhypertrophyWANGYu-bing,etal(DepartmentofCardiovascular,theAffiliatedHosp
4、ital,NorthSichuanMedicalCollege)【Abstract】Objective:ToinvestigatetheroleofAngⅡreceptors(AT1andAT2)intheleftventricularhypertrophicprocessanditsmechanismsthroughdetectingtheexpressionofAngⅡreceptors(AT1andAT2)inhypertrophiccardiomyocyteinducedbypressureoverloadinrats.Methods:FourteenMaleSpragu
5、e-Dawleyratsweredividedintotwogroups:shamgroup(n=7),andoperationgroup(n=7).Leftventricularhypertrophymodelwaswellestablishedafterabdominalaorticstenosisineachgroup.TheexpressionofAT1andAT2wasdetectedbyimmunohistochemistry(IHC)andRT-PCR,respectively.Indexesofleftventricularhypertrophy,includin
6、gmyocardialfibrosis,LVMI,cross-sectionalareaandapoptosisindex(APOI),werealsomeasured.Results:SBP,DBP,MBP,LVMI,andcardiomyocyteCSA,APOI,levelofplasmaAngⅡandexpressionofAT1andAT2inoperationgroupweremarkedlyincreasedascomparedwithshamgroup.Conclusion:ExpressionofcardiomyocyteAT1andAT2receptorswe
7、reincreasedsignificantlyinratofleftventricularhypertrophy,whichindicatedthatAT1andAT2receptorsbothparticipateintheprocessofleftventricularhypertrophybuttheymayplayantagonismeffects.【Keywords】Leftventricularhypertrophy;AngⅡ;Receptor肾素-血管紧张素系统(
