摘要
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 。
In order to investigate the relationship between cAMP and myocardial renin angiotensin system activation after acute pressure overload,an animal model of acute pressure overload was established by constriction of abdominal aorta. It was found that angiotensin converting enzyme (ACE) mRNA and protein expression were increased markedly, ACE activity and angiotensin Ⅱ content were also elevated significantly in rat heart 1 h after acute pressure overload, and the increases were kept at high level. Meanwhile the myocardial cAMP concentration was increased significantly at 0 5 h, reached the peak at day 5, and returned to normal at day 30 after operation. Then cardiomyocytes were cultured to observe whether ACE gene expression can be induced by cAMP. The results showed that elevation of cAMP content in cultured cardiomyocytes stimulated by isoproterenol (ISO, 0 01 μmol/L) increased ACE mRNA and protein expression, and also increased ACE activity and AngⅡ content in cultural medium. These results suggest that cAMP plays a role in the mechanism of activation of myocardial renin angiotensin system induced by pressure overload.
出处
《生理学报》
CAS
CSCD
北大核心
2000年第1期39-44,共6页
Acta Physiologica Sinica
基金
SupportedbytheNationalNaturalScienceFoundationofChina! (No 3960 0 0 4 1 )
