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压力负荷及容量负荷性肥厚心肌中血管紧张素Ⅱ-1型受体mRNA表达的变化 被引量:1

EXPRESSION OF ANGIOTENSIN TYPE1 RECEPTOR SUBTYPES mRAN IN MYOCARDIAL HYPERTROPHY CAUSED BY PRESSURE AND VOLUME OVERLOAD
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摘要 采用腹主动脉缩窄(AC)及腹腔动-静脉瘘(ACF)分别制造大鼠压力负荷及容量负荷增加所致心肌肥厚模型,应用反转录-聚合酶链式反应(RT-PCR)及同位素掺入技术,比较两种模型在术后不同时间点左、右心室组织中AngⅡ-1型受体a亚型(AT1a)及b亚型(AT1b)mRNA的表达及其与心肌肥厚的关系。发现AC组术后3天左室/体重比(LV/Bwt)尚未发生显著性变化,而左室组织中AT1bmRNA的表达已明显升高(P<0.01vsSO)。术后12天、35天左室肥厚进行性加重,左室组织中AT1amRNA和AT1bmRNA的表达呈进行性升高;而右室中AT1amRNA及AT1bmRNA表达始终未见升高。且右室/体重比(RV/Bwt)也始终无显著性改变。ACF组术后3d,RV/Bwt、LV/Bwt已显著升高,而左、右心室中AT1amRNA及AT1bmRNA表达尚未见显著性升高;术后12d、35d右室、左室肥厚更为明显,左、右心室组织中AT1amRNA及AT1bmRNA表达呈进行性升高。提示心肌AT1受体基因表达的变化,参与机械负荷性心肌肥厚的发生、发展,且压力负荷及容量负荷性肥厚心肌中AT1mRNA表达间的差异,可能是两种? In this study, myocardial hypertrophy caused by pressure overload (aortaconstruction,AC) and volume overload (Aortocaval fistula ACF) were duplicated on male rats ,and then we examined the expression of AT1amRNAAT1bmRNA both in left and right ventricle during different times after operation by reverse transcriptionpolymerase chain reaction(RTPCR),and isotope incorporation, in order to compare with this tow models.We found that 3 days after AC the expression of AT1bmRNA increased significantly (P<0.01 vs SO);12 days and 35 days after operation the expression of AT1amRNA and AT1bmRNA in left ventricle increased permanently with the rising of cardial mass, while the expression in right ventricle remained unchanged.3 dyas after ACF,the expression both in left and right ventricle increased obviously;12 days and 35 days after operation the expression in double ventricles increased continuously.The results suggests that the change of mRNA expression of AT1 receptor involves in the development of myocardial hypertrophy, and the difference expression of AT1 receptor between myocardial hypertrophy caused by pressure and by volume overload may be one of the reasons.The development of myocardial hypertrophy caused by pressure are different with hypertrophy by volume overload.
出处 《西安医科大学学报》 CSCD 1999年第2期155-159,170,共6页 Journal of Xi'an Medical University(Chinese)
基金 国家自然科学基金
关键词 心肌肥厚 血管紧张素Ⅱ 受体 MRNA 压力负荷 hypertrophy angiotension receptor
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  • 1Chang C,Chin J Hyper,1994年,2卷,24页

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