CAJ | 학술논문

本实验采用不同的方法复制两肾一夹(two-kidney one-clip renal hypertensive,2K1C)、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.
본실험채용불동적방법복제량신일협(two-kidney one-clip renal hypertensive,2K1C)、신경성、DOCA-염고혈압화자발성고혈압대서모형,관찰AT1A수체자신항체(AT1A-receptor autoantibodies,AT1A-AAs)재불동고혈압발병적변화규률,동시대자신항체생물활성진행분석.실험결과표명,재고혈압발병과정중AT1A-AAs적양성솔화적도균명현증가,재사충모형중,자발성고혈압조최명현,2K1C화신경성조차지.AT1A-AAs적생물활성현시,가증가배양적신생서심기세포도동빈솔화혈관수축장력.결과제시,자신면역궤제삼여료고혈압적형성,AT1A-AAs가능여심기비후유관.
Using two-kidney one-clip renal hypertensive (2K1C group), stress-induced hypertensive (neural group), DOCA-salt treated hypertensive (DOCA group) and spontaneously hypertensive rats (SHR group), to investigate the change in AT1A-receptor autoantibodies (AT1A-Aas) during the development of the four types of hypertension. The biological activities of AT1A-Aas were examined. It was shown that the frequency of occurrence and titres of AT1A-Aas increased significantly during the development of hypertension. In the four hypertensive groups studied, the occurrence of AT1A-Aas was most prominent in SHR, 2K1C and neural groups. The biological effects of AT1A-Aas were shown to increase the beating frequency of cultured neonatal myocardial and vascular contractile tension. It is suggested that autoimmune mechanisms are involved the pathogenesis of different types of hypertension and the AT1A-Aas may be one of the mechanisms leading to cardiac hypertrophy.