L-精氨酸和一氧化氮抑制剂对大鼠血管钙化的影响  

Effects of L-Arginine and nitric oxide inhibitor on vascular calcification in rats

作　　者：张宝红[1] 吴胜英[2] 庞永正[3] 李菊香[3] 唐朝枢[3] 杜军保[1] 

机构地区：[1]北京大学第一医院儿科研究室,北京100034 [2]郧阳医学院病生教研室,十堰442000 [3]北京大学第一医院心血管研究所,北京100034

出　　处：《基础医学与临床》2003年第6期599-603,共5页Basic and Clinical Medicine

基　　金：国家重点基础研究发展规划项目 (G2 0 0 0 0 5 6 90 5 );中华人民共和国教育部特殊教育发展基金 (985 )

摘　　要：观察给予一氧化氮合酶 (NOS)的抑制剂左旋硝基精氨酸 (L NNA)或底物L -精氨酸 (L Arg)对血管钙化的影响。利用维生素D3 和尼古丁制备大鼠血管钙化模型 ,测定大鼠尾动脉压 ,血管钙含量、碱性磷酸酶活性及45Ca沉积 ;并检测血管组织的L Arg转运 ,NOS活性及NO2 -和cGMP含量。发现钙化大鼠血压略升高 ;动脉钙含量、ALP活性及45Ca沉积明显增加 ,vonKossa染色可以看到明显的钙化颗粒 ;钙化血管组织NOS活性升高 ;NO和cGMP含量均减少。给予L NNA或L Arg后 ,与单纯钙化组相比 ,L NNA干预组的L Arg转运、NOS活性及NO和cGMP的含量均降低 ;而L Arg干预组上述指标的变化正相反。同时 ,L NNA干预组的钙化程度比钙化组加重 ,而L Arg干预组的钙化程度比钙化组减轻 ;提示血管钙化时NO NOS cGMP途径发生紊乱 ,干预NO NOSTo explore the role of L-Arginine(L-Arg)/NO pathway in vascular calcification and the effects of L-NNA and L-Arg on vascular calcification, vascular calcification model was established in rats (VND group) by administrating vitamin D 3 and nicotine. The blood pressure of animals was measured, and vascular calcium content, alkaline phosphatase (ALP) activity and 45Ca deposition were detected. The velocity of L-Arg transport, the activity of nitric oxide synthase (NOS) and the product of NO 2 - and cGMP in aorta were determined in each group. In comparison of control group, the blood pressure of rats with vascular calcification were slightly increased, and the vascular calcium content, ALP activity and 45Ca deposition in calcified group were obviously increased. The velocity of L-Arg transport was lowered, NOS activity increased, and NO and cGMP content decreased in calcified group. When L-NNA or L-Arg was added, the velocity of L-Arg transport, NOS activity NO and cGMP content in VDN+L-NNA group were significantly lower than that in calcified group, and the above four markers were higher in VDN+L-Arg group than those in calcified group. Contrary to that, the vascular calcium content, ALP activity and 45Ca deposition in VDN+L-NNA group were significantly higher than calcified group, but decreased in VDN+L-Arg group. The results showed that there were disorders in L-Arg-NOS-NO-cGMP pathway in calcified vessels, and we could influence vascular calcification by intervening L-Arg-NOS-NO-cGMP pathway.

关 键 词：L-精氨酸 一氧化氮抑制剂 大鼠 血管钙化 一氧化氮合酶 左旋硝基精氨酸 环磷酸鸟苷 

分 类 号：R965[医药卫生—药理学]