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心房颤动患者心房组织的血管紧张素转换酶2表达及血管紧张素转换酶抑制剂干预的影响
引用本文:Hu XS,Xie XD,Wang XX,Zeng CL,Ni YM,Yu GW,Chen JZ. 心房颤动患者心房组织的血管紧张素转换酶2表达及血管紧张素转换酶抑制剂干预的影响[J]. 中华心血管病杂志, 2007, 35(7): 625-628
作者姓名:Hu XS  Xie XD  Wang XX  Zeng CL  Ni YM  Yu GW  Chen JZ
作者单位:1. 浙江大学医学院附属第一医院心内科,杭州,310003
2. 浙江大学医学院附属第一医院胸外科,杭州,310003
摘    要:
目的 探讨心房颤动(房颤)患者心房肌组织中血管紧张素转换酶2(ACE2)的表达和血管紧张素转换酶抑制剂(ACEI)干预的影响及可能的信号传导途径。方法 选取接受开胸手术的风湿性心脏病患者47例,手术中取右心耳处心房肌标本。采用RT-PCR法检测心房肌ACE2和ACEmRNA水平,采用Western blot法检测ACE、ACE2、细胞外信号调节激酶1/2(ERK1/2)和磷酸化的细胞外信号调节激酶1/2(pERK1/2)蛋白表达水平,应用放射免疫法检测心房肌组织血管紧张素Ⅱ(AngⅡ)水平。结果 与窦性心律组相比,持续性房颤组心房肌组织中ACE2表达显著减少(P〈0.05),而ACE的表达和AngⅡ含量显著增加(P〈0.05)。ERK1/2的活化水平在持续性房颤组较窦性心律组明显增加(P〈0.05)。与持续性房颤组相比,ACEⅠ干预组ACE2表达水平显著增加(P〈0.01),ERK1/2的活化水平显著降低(P〈0.05),而ACE表达和AngⅡ含量差异无统计学意义。结论 房颤患者心房肌组织中ACE2表达下调,ACE/ACE2平衡失调;ACEⅠ对房颤的长期临床效应可能与其上调ACE2、抑制有丝分裂素激活蛋白激酶信号途径有关。

关 键 词:心房颤动 肽基二肽酶A 血管紧张素转换酶抑制药 有丝分裂素激活蛋白激酶类
修稿时间:2006-08-21

Effects of angiotensin converting enzyme inhibitor on the expression of angiotensin converting enzyme 2 in atrium of patients with atrial fibrillation
Hu Xiao-sheng,Xie Xu-dong,Wang Xing-xiang,Zeng Chun-lai,Ni Yi-ming,Yu Guo-wei,Chen Jun-zhu. Effects of angiotensin converting enzyme inhibitor on the expression of angiotensin converting enzyme 2 in atrium of patients with atrial fibrillation[J]. Chinese Journal of Cardiology, 2007, 35(7): 625-628
Authors:Hu Xiao-sheng  Xie Xu-dong  Wang Xing-xiang  Zeng Chun-lai  Ni Yi-ming  Yu Guo-wei  Chen Jun-zhu
Affiliation:Department of Cardiology, First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, China
Abstract:
OBJECTIVE: To investigate the expression of angiotensin converting enzyme 2 (ACE2) and the changes treated with angiotensin converting enzyme inhibitor (ACEI), and its signal transduction pathway. METHODS: Atrial tissues were obtained from 47 patients with RHD undergoing cardiac surgery. The mRNA of ACE2 and ACE were semi-qualified by RT-PCR and normalized to the gene beta-actin. Western blot analysis was employed to examine the expressions of ACE2, ACE, ERK1/2 and phosphorylated ERK (pERK1/2). The atrial tissue angiotensin II (Ang II) content was determined by radioimmunoassay detection. RESULTS: The expression of ACE2 was significantly decreased (P < 0.05), the expression of ACE and pERK1/2 were significantly increased (P < 0.05), and the level of atrial tissue Ang II was significantly increased in patients with chronic atrial fibrillation group (CAF) compared with sinus rhythm group (SR) (P < 0.05). Compared with CAF patients treated without ACEI, the expression of ACE2 significantly increased (P < 0.01), and the relative activity of ERK1/2 significantly decreased (P < 0.05), whereas the expression of ACE and the level of atrial tissue Ang II remained unchanged in CAF patients treated with ACEI. CONCLUSIONS: The study suggested that the dysequilibrium of ACE/ACE2 might play an important role in the process of atrial fibrillation, which may be related to the activation of ERK1/2 pathway. The clinical effect of long-term treatment of ACEI maybe associated with elevated ACE2 expression but not ACE expression.
Keywords:Atrial fibrillation   Peptidyl-dipeptidase A   Angiotensin-converting enzyme inhibitors   Mitogen-activated protein kinases
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