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目的 :在大鼠血管钙化模型上观察内源性血管紧张素II(AngⅡ )对大鼠血管钙化的影响。方法 :用VitD3 皮下注射和尼古丁灌胃诱导大鼠血管钙化模型。测定血管组织中钙含量、[45Ca2 + ]聚集及碱性磷酸酶活性作为观察钙化的指标。结果 :钙化血管组织中钙含量 ,[45Ca2 + ]摄入及碱性磷酸酶活性分别高于对照组。血管组织中的血管紧张素原mRNA、血浆和血管AngⅡ含量均高于对照组水平。血管紧张素转换酶抑制剂卡托普利和AngⅡ受体AT1阻断剂洛沙坦处理的大鼠血管内钙含量、[45Ca2 + ]聚集及碱性磷酸酶活性显著低于单纯钙化组。卡托普利处理的钙化大鼠血浆和动脉中AngⅡ含量、动脉中血管紧张素原mRNA的含量也显著低于钙化组水平。结论 :钙化大鼠血浆和血管组织中AngⅡ水平上调 ,卡托普利和洛沙坦可减轻大鼠血管钙化程度
OBJECTIVE: To observe the effect of endogenous angiotensin II (AngⅡ) on vascular calcification in rat vascular calcification model. Methods: The vascular calcification model was induced by subcutaneous injection of VitD3 and nicotine. The contents of calcium in blood vessel, [45Ca2 +] accumulation and alkaline phosphatase activity were measured as indicators of calcification. Results: Calcium content, [45Ca2 +] uptake and alkaline phosphatase activity in calcified vascular tissue were higher than those in control group respectively. Angiotensinogen mRNA, plasma and vascular Ang II levels in vascular tissue were higher than the control group. Angiotensin converting enzyme inhibitor captopril and angiotensin II receptor AT1 antagonist Losartan treatment of intravascular calcium content, [45Ca2 +] accumulation and alkaline phosphatase activity was significantly lower than the simple calcification group. Captopril treatment of calcified rat plasma and artery Ang Ⅱ content, arterial angiotensinogen mRNA content was significantly lower than the level of calcification group. Conclusion: The level of AngⅡ in plasma and vascular tissue of calcified rats is up-regulated. Captopril and losartan can reduce the degree of vascular calcification