中文摘要：

目的观察快速心房起搏模型犬血管紧张素转换酶2（ACE2）和血管紧张素III型受体（ATlR）mRNA表达的变化，以及应用依那普利、厄贝沙坦及血管紧张素（Ang）-（1-7）对其影响。方法健康成年杂种犬30只，分为5组：假手术组（S组），心房起搏对照组（C组），心房起搏＋依那普利组（EN组），心房起搏＋厄贝沙坦组（IB组），心房起搏＋血管紧张素-（1-7）组（A组），每组6只。S组植入起搏器，但不行起搏刺激及药物干预。C组植入起搏器并起搏，但无药物干预。EN组及IB组分别于起搏开始前3d开始给予口服依那普利2mg·kg^-1·d^-1或厄贝沙坦60mg·kg^-1·d^-1。A组给予Ang-（1-7）6μg·kg^-1·h^-1持续静脉泵人。各组犬经500次／min快速心房起搏2周后，采集右心房肌标本，逆转录聚合酶链式反应（RT—PCR）检测心房肌组织中ACE2和ATlRmRNA表达。结果心房起搏组较假手术组ACE2表达降低，ATlR表达明显升高，应用依那普利、厄贝沙坦和Ang－（1-7）可使ACE2表达增加和ATIR水平下调。结论快速心房起搏2周可诱发心脏局部肾素－血管紧张素（RAS）系统的活化，依那普利、厄贝沙坦和Ang－（1-7）可抑制起搏后的RAS系统激活，降低心房颤动的易感性。Ang－（1-7）的心脏保护作用可能通过下调ATIR和上调ACE2来介导。

英文摘要：

Objective To investigate the mRNA expression of angiotensin converting enzyme 2 （ACE2） and angiotensin II type 1 receptor（ AT1 R） in a canine model of rapid atrial pacing and the effects of enalapril, irbesmtan and angiotensin-（ 1-7 ） on ACE2 and ATI R expression. Methods Thirty mongrel dogs were assigned to the sham-operated group （ S, n = 6）, pacing-control group （ C, n = 6 ）, pacing and enalapriltreated group（ EN, n = 6 ） , pacing and irbesartan-treated group （ IB, n = 6 ） or pacing and Ang-（ 1-7 ） -treated group（A, n = 6）. The rapid atrial pacing at 500 beats per minute was maintained for 2 weeks except sham group. The dogs in the EN, IB and A groups respectively received enalapril （2 mg· kg^-1· d^-1 ）, irbesartan （ 60 mg· kg ^- 1· d^ - 1 ） orally or Ang- （ 1-7 ） （ 6 μg · kg ^- 1 . h^ - 1 ） intravenously during the pacing period. RTPCR was applied to assess the mRNA expression of ACE2 and AT1R in right atrial tissue. Result In the pacing-control group, ACE2 mRNA expression was declined and AT1R expression was markedly elevated than sham group. Enalapril, irbesartan or angiotensin-（ 1-7 ） treatement caused increased ACE2 mRNA expression and decreased AT1R expression in comparison with the pacing-control group. Conclusion Chronic rapid atrial pacing leads to renin angiotensin system activation which is contributed to the atrial fibrillation. Enalapril,irbesartan and angotensin- （ 1-7 ） can suppress the activation of RAS, thereby reducing the atrial fibrillation vulnerability. The cardiac protection of angiotcnsin-（ 1-7 ） probably is mediated by the downregulation of AT1R and increased ACE2 expression.