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目的探讨替米沙坦对压力负荷过重所致心衰大鼠血管紧张素Ⅱ(AngⅡ)、心肌血管紧张素Ⅱ1型受体(AT1R)、血管紧张素转化酶2(ACE2)及MAS蛋白表达的影响。方法采用SD雄性大鼠通过腹主动脉缩窄术构建压力负荷性心肌肥厚致心力衰竭(HF)模型。将大鼠随机分为假手术对照组(n=12)、HF模型组(n=12)和替米沙坦干预组(n=12)。替米沙坦干预组每天给予替米沙坦连续8周,检测各组大鼠血流动力学参数、心脏指数、血浆AngⅡ含量、心肌中AT1R、ACE2和MAS蛋白的表达情况。结果 HF模型组心脏指数、血流动力学指标、血浆AngⅡ的含量及心肌AT1R、ACE2蛋白的表达明显升高(P<0.01),MAS蛋白表达明显下降(P<0.01);替米沙坦干预组心脏指数、血流动力学指标明显下降(P<0.01),血浆AngⅡ的含量及心肌AT1R蛋白的表达明显下降(P<0.01),而MAS和ACE2蛋白的表达明显升高(P<0.01)。结论应用替米沙坦可明显改善HF大鼠心室重构,可能与AngⅡ和AT1R的下调,而MAS和ACE2的上调有关。
Objective To investigate the effects of telmisartan on the expression of angiotensin Ⅱ (AngⅡ), angiotensin Ⅱ type 1 receptor (AT1R), angiotensin Ⅱ converting enzyme 2 (ACE2) and MAS protein in heart failure rats under pressure overload. Impact. Methods SD male model of hypertensive heart failure (HF) was established by abdominal aorta constriction. The rats were randomly divided into sham operation control group (n = 12), HF model group (n = 12) and telmisartan intervention group (n = 12). The telmisartan intervention group was given telmisartan every day for 8 consecutive weeks. The hemodynamic parameters, cardiac index, plasma AngⅡ, the expression of AT1R, ACE2 and MAS in myocardium were detected. Results The cardiac index, hemodynamics, AngⅡ and the expression of AT1R and ACE2 in HF group were significantly increased (P <0.01), and the expression of MAS protein was significantly decreased (P <0.01) (P <0.01). The content of AngⅡ and the expression of AT1R in myocardium were significantly decreased (P <0.01), while the expressions of MAS and ACE2 were significantly increased (P <0.01) . Conclusion Telmisartan can significantly improve ventricular remodeling in HF rats, which may be related to the down-regulation of AngⅡ and AT1R, while upregulation of MAS and ACE2.