论文部分内容阅读
血管紧张素Ⅱ(AngⅡ)是肾素-血管紧张素系统中最主要的活性物质,与受体结合后可激活蛋白激酶C(PKC),活化的PKC可以通过各种信号转导途径,促进心肌成纤维细胞增殖,诱导心肌纤维化,导致心室重构。血管紧张素Ⅱ受体(AT1受体)拮抗剂,可以阻滞AngⅡ促心血管细胞增殖肥大作用,同时AT1受体被阻断后,反馈性地使血浆肾素增加2～3倍,导致血浆中的AngⅡ浓度升高。由于AT1受体已经被阻滞,这些反馈作用难以表现。但血浆中升高的AngⅡ通过激活AT2受体,进而激活缓激肽-一氧化氮途径,产生舒张血管、降低血压、抑制心血管重构等作用。
Angiotensin Ⅱ (AngⅡ), the most important active substance in renin-angiotensin system, activates protein kinase C (PKC) when it binds to the receptor. Activated PKC can promote myocardial transport through a variety of signal transduction pathways Fibroblast proliferation, induced myocardial fibrosis, leading to ventricular remodeling. Angiotensin Ⅱ receptor (AT1 receptor) antagonists, can block Ang Ⅱ promote cardiovascular hypertrophy, while AT1 receptor is blocked, the feedback plasma renin increased 2 to 3 times, leading to plasma In the Ang Ⅱ concentration increased. Since AT1 receptors have been blocked, these feedback effects are difficult to show. However, elevated Ang II in plasma activates the AT2 receptor, which in turn activates the bradykinin-nitric oxide pathway, resulting in vasodilation, hypotension, and cardiovascular remodeling.