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目的:我们以往研究证实,机械牵张可不依赖于血管紧张素Ⅱ(AngⅡ)独立活化其1型受体(AT1-R),并介导细胞内信号转导参与心肌重构反应,然而内在的分子机制不明,通过体外培养的心肌细胞和在体的血管紧张素原基因敲除(AGT KO)
OBJECTIVE: Our previous studies confirmed that mechanical stretch independently relies on angiotensin Ⅱ (AT1-R) to activate its type 1 receptor (AT1-R) and mediate intracellular signal transduction to participate in myocardial remodeling, whereas intrinsic stretch The molecular mechanism is not clear, through in vitro cultured cardiomyocytes and in vivo angiotensinogen gene knockout (AGT KO)