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首页> 外文期刊>American Journal of Physiology >Interaction between AT1 and AT2 receptors during postinfarction left ventricular remodeling.
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Interaction between AT1 and AT2 receptors during postinfarction left ventricular remodeling.

机译：梗死后左心室重构中AT1和AT2受体之间的相互作用。

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摘要

The relative contribution of the angiotensin II type 1 and 2 receptors (AT1-R and AT2-R) in postmyocardial infarction (MI) remodeling remains incompletely understood. We studied five groups of C57Bl/6 mice after 1 h of left anterior descending artery occlusion-reperfusion: 1) wild type, untreated (n = 12); 2) wild type, treated with the AT1-R blocker losartan (10-20 mg.kg(-1).day(-1) in drinking water) from day 1 to day 28 post-MI (n = 10); 3) cardiac overexpression of the AT2-R [AT2-transgenic (TG); n = 14]; 4) AT2-TG treated with losartan (n = 13); and 5) AT2-TG and null for the AT1a-R [AT2-TG/AT1 knockout (KO); n = 10]. Cardiac magnetic resonance imaging (CMR) measured ejection fraction and left ventricular end-diastolic and end-systolic volume (EDVI and ESVI) and mass indexed to weight on days 0, 1, 7, and 28 post-MI. Infarct size was measured on day 1 by late gadolinium-enhanced CMR. Regional myocyte hypertrophy and collagen content were measured on day 28 post-MI. Infarct size was similar among groups. Systolic blood pressure was lowest in AT2-TG/AT1KO. By day 28 post-MI, when corrected for baseline differences, EDVI and ESVI were higher and ejection fraction was lower in wild type than other groups. Ejection fraction was highest and EDVI and mass index were lowest in AT2-TG/AT1KO at day 28. The AT2-TG/AT1KO demonstrated less fibrosis in adjacent regions. Regional myocyte hypertrophy was similar in all groups. The AT1-R and AT2-R are intricately intertwined in post-MI remodeling. Pharmacological blockade of AT1-R is equivalent to AT2-R overexpression in attenuating post-MI remodeling. Genetic knockout of the AT1a-R is additive to AT2-R overexpression, due, at least in part, to blood pressure lowering.
机译：尚不完全了解血管紧张素II 1型和2型受体（AT1-R和AT2-R）在心肌梗塞后（MI）重塑中的相对作用。在左前降支再灌注1小时后，我们研究了五组C57Bl / 6小鼠：1）野生型，未经治疗（n = 12）; 2）野生型，在心梗后第1天至第28天用AT1-R阻断剂氯沙坦（10-20 mg.kg（-1）.day（-1）在饮用水中）处理; 3）AT2-R [AT2-转基因（TG）的心脏过表达; n = 14]; 4）用氯沙坦处理的AT2-TG（n ＝ 13）; 5）AT2-TG，AT1a-R [AT2-TG / AT1敲除（KO）为空; n = 10]。心肌磁共振成像（CMR）在心梗后第0、1、7和28天测量了射血分数，左心室舒张末期和收缩末期体积（EDVI和ESVI），并以重量作为质量指标。在第1天通过晚期late增强的CMR测量梗死面积。在MI后第28天测量局部肌细胞肥大和胶原蛋白含量。各组间梗死面积相似。收缩压最低的是AT2-TG / AT1KO。心肌梗死后第28天，经校正基线差异后，野生型的EDVI和ESVI较高，而射血分数则低于其他组。在第28天，AT2-TG / AT1KO的射血分数最高，而EDVI和质量指数最低。AT2-TG/ AT1KO在相邻区域的纤维化较少。所有组的区域性心肌细胞肥大均相似。在MI后重塑中，AT1-R和AT2-R错综复杂地交织在一起。在减缓心梗后重塑中，AT1-R的药理学阻断作用等同于AT2-R的过表达。 AT1a-R的基因敲除是至少部分归因于血压降低的AT2-R过表达的补充。

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