心房颤动患者心房组织血管紧张素Ⅱ受体表达及血管紧张素转换酶抑制剂干预的初步研究

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目的探讨心房颤动(房颤)患者心房组织血管紧张素Ⅱ(AngⅡ)受体基因转录和蛋白表达的变化以及血管紧张素转换酶抑制剂(ACEI)干预的影响。方法45例心脏外科手术患者,其中窦性心律和房颤患者各12例,应用低剂量ACEI的窦性心律和房颤患者分别为9例和12例。取右心耳组织通过逆转录聚合酶链反应和免疫组织化学技术测量血管紧张素Ⅱ1型受体(AT1)和血管紧张素Ⅱ2型受体(AT2)mRNA和蛋白的相对表达量。结果窦性心律和房颤患者之间的心房组织AT1和AT2mRNA表达量差异无统计学意义;房颤患者心房组织AT1蛋白表达量明显低于窦性心律患者(2.63±1.00vs4.64±1.48,P<0.001),AT2蛋白表达量明显高于窦性心律患者(6.20±2.17vs3.72±0.88,P<0.05);应用低剂量ACEI的窦性心律和房颤患者分别与未应用ACEI的窦性心律和房颤患者相比,AT1和AT2的mRNA和蛋白表达量差异无统计学意义。结论房颤时AT1蛋白表达下调,AT2蛋白表达上调,相应的mRNA表达水平差异无统计学意义,提示肾素血管紧张素系统参与了房颤的心房结构重构;低剂量ACEI不能逆转房颤AngⅡ受体重构。 Objective To investigate the changes of angiotensin Ⅱ (Ang Ⅱ) receptor gene transcription and protein expression in atrial fibrillation (AF) patients and the intervention of angiotensin converting enzyme inhibitor (ACEI). Methods A total of 45 patients undergoing cardiac surgery, including 12 patients with sinus rhythm and atrial fibrillation, had 9 patients with sinus rhythm and 12 patients with atrial fibrillation undergoing ACEI. The right atrial appendage tissues were used to measure the mRNA and protein expressions of AT1 and AT2 by reverse transcription polymerase chain reaction and immunohistochemistry. Results There was no significant difference in AT1 and AT2 mRNA expression between atrial fibrillation patients and atrial fibrillation patients. Atrial AT1 protein expression in atrial fibrillation patients was significantly lower than that in sinus rhythm patients (2.63 ± 1.00 vs 4.64 ± 1.48, (P <0.001). The expression of AT2 protein was significantly higher in patients with sinus rhythm (6.20 ± 2.17 vs 3.72 ± 0.88, P <0.05). Compared with patients without ACEI Compared with patients with atrial fibrillation, there was no significant difference in mRNA and protein expression of AT1 and AT2 between patients with atrial fibrillation and patients with atrial fibrillation. Conclusions AT1 protein expression is down-regulated and AT2 protein is up-regulated in atrial fibrillation with no significant difference in mRNA expression, suggesting that renin-angiotensin system is involved in atrial structural remodeling of atrial fibrillation. Low-dose ACEI can not reverse AngⅡ Reconfiguration of receptors.
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