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Attenuation of Myocardial Stunning by Angiotensin II Type 1 Receptor Blockade with Candesartan: Role of the Type 2 Receptor

机译:血管紧张素II型1受体封闭因子的抗心肌壮丽的衰减:2型受体的作用

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We assessed the effect of the angiotensin II (Angll) type 1 receptor (AT_1R) blocker, candesartan on hemodynamics and LV systolic and diastolic function, infarct size and regional AT_1R and Angll type 2 receptor (AT_2R) proteins after regional anterior ischemia-reperfusion (IR) (60 min ischemia, 90 min reperfusion) in Sprague-Dawley rats randomized to intravenous candesartan or saline (control) before IR. Compared to the controls, candesartan significantly (P<0.001) decreased infarct size, limited increases in left atrial pressure, improved positive and negative LV dP/dt, normalized ejection fraction, improved diastolic function, limited infarct expansion and increased AT,R protein in the reperfused zone, with no change in AT_1R after IR. The results suggest that AT_2R upregulation during AT_1R blockade might contribute in limiting myocardial stunning during IR in the rat.
机译:我们评估了血管紧张素II(Angll)1型受体(AT_1R)阻断剂,在血流动力学和LV收缩和舒张功能,梗塞大小和区域AT_1R和ANGL1型受体(AT_2R)蛋白在区域前缺血再灌注( IR)(60分钟缺血,90分钟再灌注)在Sprague-Dawley大鼠随机化以前IR之前的静脉内坎糖或盐水(对照)。与对照相比,CandaArtan显着(P <0.001)降低梗塞尺寸,左心压有限,左侧心脏压力的增加,阳性和阴性LV DP / DT,归一化射血分数,改善的舒张功能,有限的梗塞功能,有限的梗塞膨胀和增加,R蛋白再灌注区域,IR后没有变化的AT_1R。结果表明,在AT_1R封锁期间的AT_2R上调可能有助于限制在R大鼠中的IR期间的心肌令人震惊。

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