摘要
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 。
AIM: To explore the effects of angiotensin II on aortic calcification in the rat. METHODS: Arterial calcification of Sprague-Dawley rats was induced by vitamin D_3 plus nicotine. Calcification was confirmed by Von Kossa staining, measurement of calcium content, [^(45)Ca^(2+)] accumulation and alkaline phosphatase (ALP) activity of vascular tissue. RESULTS: The results showed that calcium content, [^(45)Ca^(2+)] accumulation and ALP activity in calcified arteries increased significantly compared with those of control. Ang Ⅱ levels in plasma and aortic tissues and the amount of angiotensinogen mRNA in calcified aorta were also increased as compared with control. Captopril (inhibitor of ACE) and losartan (Ang Ⅱ receptor inhibitor) decreased significantly the content of calcium, [^(45)Ca^(2+)] uptake and ALP activity in calcified aorta. Ang Ⅱ levels in plasma and aortic tissues and the amount of angiotensinogen mRNA in aortic tissue were down-regulated by captopril. The amount of angiotensinogen mRNA and the content of Ang Ⅱ in the calcified aorta were also decreased by losartan. CONCLUSION: The captopril and losartan significantly alleviate the vascular calcification. [
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2004年第11期1961-1965,共5页
Chinese Journal of Pathophysiology
基金
国家重大基础研究发展规划项目 (973)(G2 0 0 0 0 5 6 90 5 )资助
北京大学医学部"985计划"项目基金(985 )资助
关键词
血管紧张索Ⅱ
卡托普利
洛沙坦
血管
钙化
Angiotensin II
Captopril
Losartan
Blood vessels
Calcification
