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为阐明急性压力超负荷后心肌细胞内cAMP浓度升高和心肌肾素血管紧张素系统活化之间是否存在内在因果联系 ,用腹主动脉缩窄的方法建立急性压力超负荷大鼠模型。发现在术后 1h心肌组织中血管紧张素转换酶 (ACE)mRNA及蛋白表达均显著增加 ,ACE活性及血管紧张素Ⅱ (AngⅡ )含量也明显升高 ,并持续在高水平。同时 ,心肌组织cAMP含量于术后 0 5h明显增加 ,术后 5d时达峰值 ,术后 3 0d降至正常。在心肌细胞培养的基础上 ,用异丙肾上腺素 (ISO)刺激培养心肌细胞 ,升高细胞内cAMP浓度 ,发现 0 0 1μmol/LISO即可刺激心肌细胞使ACEmRNA及蛋白表达显著增加 ,并使ACE活性和AngⅡ含量增加。在体和离体实验结果提示 ,cAMP与压力超负荷后血管紧张素转换酶基因表达有关
To clarify whether there is an internal causal relationship between the increase of cAMP concentration in cardiac myocytes and the activation of cardiac renin-angiotensin system after acute pressure overload, an acute pressure overload rat model was established by abdominal aorta constriction. It was found that the mRNA and protein expression of angiotensin converting enzyme (ACE) increased significantly at 1 hour after operation, and the activity of ACE and the content of angiotensin Ⅱ (Ang Ⅱ) were also significantly increased. At the same time, the cAMP content in myocardial tissue increased significantly at 0 h after operation and peaked at 5 d after operation. The level of cAMP decreased to normal at 30 d after operation. On the basis of cardiomyocyte culture, myocardial cells were cultured with isoprenaline (ISO) and the intracellular cAMP concentration was increased. It was found that 0 0 1μmol / L ISO stimulated cardiomyocytes to significantly increase ACE mRNA and protein expression, Activity and Ang Ⅱ content increased. In vivo and in vitro results suggest that cAMP is associated with angiotensin-converting enzyme gene expression after pressure overload