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近年来发现内皮素 (ET1)除具有强大的缩血管作用外 ,还是一个强大的致心肌肥大活性因子。为探讨(ET1)在运动性心肌肥大形成中的作用 ,本实验采用免疫组化和Northern分子杂交方法 ,对游泳运动大鼠和自发性高血压大鼠 (SHR)心肌细胞ET1分布及其基因表达进行研究。结果表明 :大鼠经 10周游泳运动后心肌细胞ET1分布和mRNA表达均比安静对照大鼠增加 ,但比安静SHR心肌细胞ET1分布和mRNA表达减少 ;SHR经 10周游泳运动后 ,心肌细胞ET1分布和mRNA表达均比安静SHR明显降低。这些结果提示 :( 1)ET1参与运动性心肌肥大形成机制 ,并在其变化特征上与高血压肥大心脏不同 ;( 2 )运动使高血压肥大心肌细胞ET1分布减少 ,在减轻ET1对肥大心脏的损伤作用方面可能具有积极意义 ;( 3 )运动可在基因转录水平上调节心肌细胞内ET1分布变化。
In recent years, endothelin (ET1) has been found to be a potent inducer of cardiac hypertrophy in addition to its potent vasoconstrictor effect. In order to explore the role of ET1 in the development of exercise-induced cardiac hypertrophy, ET1 distribution and gene expression in cardiomyocytes of swimming and spontaneous hypertensive rats (SHR) were detected by immunohistochemistry and Northern blot hybridization research. The results showed that ET1 distribution and mRNA expression in cardiomyocytes of rats after swimming for 10 weeks were higher than those in quiet control rats, but the distribution and mRNA expression of ET1 in myocardial cells were decreased after SHR swimming for 10 weeks. ET1 Distribution and mRNA expression were significantly lower than the quiet SHR. These results suggest that: (1) ET1 participates in the mechanism of exercise-induced cardiac hypertrophy and is different from hypertensive hypertensive heart in its changing features; (2) Exercise reduces the ET1 distribution in hypertrophic cardiomyocytes, Injury may have positive significance; (3) Exercise can regulate the distribution of ET1 in myocardial cells at the level of gene transcription.