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本实验采用不同的方法复制两肾一夹(two-kidney one-clip renal hypertensive,2KIC)、神经性、DOCA-盐高血压和自发性高血压大鼠模型,观察AT1A受体自身抗体(AT1A-receptor autoantibodies,AT1A-AAs)在不同高血压发病的变化规律,同时对自身抗体生物活性进行分析。实验结果表明,在高血压发病过程中AT1A-AAs的阳性率和滴度均明显增加,在四种模型中,自发性高血压组最明显,2K1C和神经性组次之。AT1A-AAs的生物活性显示,可增加培养的新生鼠心肌细胞跳动频率和血管收缩张力。结果提示,自身免疫机制参与了高血压的形成,AT1A-AAs可能与心肌肥厚有关。
In this study, we used two different methods to replicate two-kidney one-clip renal hypertensive (2KIC), neurogenic, DOCA-salt hypertensive and spontaneous hypertensive rat models. AT1A- receptor autoantibodies, AT1A-AAs) in the pathogenesis of hypertension. Meanwhile, the bioactivity of autoantibodies was analyzed. The experimental results showed that the positive rate and titer of AT1A-AAs were significantly increased in the pathogenesis of hypertension. Among the four models, the spontaneous hypertension group was the most obvious, followed by 2K1C and neurotic group. The biological activity of AT1A-AAs has been shown to increase the beating frequency and vasoconstriction tension of cultured neonatal rat cardiomyocytes. The results suggest that autoimmune mechanism involved in the formation of hypertension, AT1A-AAs may be related to cardiac hypertrophy.