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目的探讨大鼠血浆肾素-血管紧张素-醛固酮系统(RAAS)在高原低氧习服过程中的作用及其右心室血管紧张素转换酶2(ACE2)表达变化。方法将40只雄性SD大鼠随机分为4组,分别为缺氧1、3、30d组,对照组(西安地区海拔5 m);3个缺氧组动物由西安耗时1 d带到青海格尔木(海拔2 700 m)、3 d带到西藏那曲(海拔4 500 m)及那曲饲养30 d,用放射免疫法测定大鼠血浆肾素(PRA),血管紧张素Ⅱ(ATⅡ),醛固酮(ALD)的浓度,采用逆转录-聚合酶链反应(RT-PCR),免疫印迹、(western blot)检测各组大鼠心脏右心室心肌ACE2mRNA、蛋白水平的表达变化。结果缺氧1d组血浆PRA含量为每小时(5.15±0.86)ng/mL,ATⅡ、ALD含量分别为(92.10±10.25)、(85.60±29.40)pg/mL;缺氧3、30 d组血浆PRA含量分别为每小时(7.12±0.31)和(5.37±0.28)ng/mL,ATⅡ、ALD含量分别为(160.53±10.84)、(127.45±30.6)和(56.30±25.23)、(82.54±26.78)pg/mL;缺氧30 d组右心室明显肥大伴右心功能明显上调,同时右心室ACE2 mRNA、蛋白合成均有明显增加(P<0.01)。结论高原缺氧大鼠RAAS在高原习服中参与并发挥重要作用,慢性高原低氧环境下大鼠心肌组织ACE2 mRNA、蛋白水平显著上调。
Objective To investigate the role of plasma renin-angiotensin-aldosterone system (RAAS) in rats during hypoxia acclimation and the expression of angiotensin-converting enzyme 2 (ACE2) in rat right ventricle. Methods Forty male Sprague-Dawley rats were randomly divided into 4 groups: hypoxia 1, 3 and 30 days, and control group (5 m above sea level in Xi’an). Three hypoxia groups were brought to Qinghai Golmud (2 700 m), 3 days to Nagqu, Tibet (elevation 4 500 m), and Nagqu were housed for 30 days. The contents of plasma renin (PRA), angiotensin Ⅱ (ATⅡ), aldosterone ALD). The expression of ACE2 mRNA and protein in right ventricular myocardium of rats in each group were detected by RT-PCR, western blot and western blot. Results The level of PRA in hypoxia group was (5.15 ± 0.86) ng / mL per hour, and the levels of ATⅡ and ALD were (92.10 ± 10.25) and (85.60 ± 29.40) pg / mL respectively (7.12 ± 0.31) and (5.37 ± 0.28) ng / mL respectively, and the contents of ATⅡ and ALD were (160.53 ± 10.84), (127.45 ± 30.6) and (56.30 ± 25.23) and (82.54 ± 26.78) pg / mL; right ventricular hypertrophy and right ventricular function were significantly increased in hypoxia 30 d group, while right ventricular ACE2 mRNA and protein synthesis were significantly increased (P <0.01). Conclusions RAAS plays an important role in plateau acclimatization in rats with plateau hypoxia. ACE2 mRNA and protein levels are significantly up-regulated in rats with chronic high altitude hypoxia.