血管紧张素Ⅱ受体拮抗药对大鼠血管平滑肌细胞增殖的影响  被引量:1

The Affection of Angiotensin Ⅱ Antagonists on the Proliferation of Rat Vascular Smooth Muscle Cells

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作  者:郑汉巧[1] 董传仁[1] 汪长华[1] 李端详[1] 欧阳静萍[1] 涂淑珍[1] 李柯[1] 

机构地区:[1]武汉大学医学院病理生理教研室,430071

出  处:《医药导报》2001年第6期341-342,共2页Herald of Medicine

基  金:国家自然科学基金资助课题 (批号 3960 0 0 59)

摘  要:目的 :利用血管紧张素Ⅱ受体拮抗药洛沙坦、PD12 3319研究血管紧张素Ⅱ 2型受体对培养的大鼠主动脉平滑肌细胞增殖的影响。方法 :将含有血管紧张素Ⅱ 2型受体cDNA的质粒转染入培养的大鼠主动脉平滑肌细胞后 ,实验组分为血管紧张素Ⅱ处理组 (组 1)、血管紧张素Ⅱ和洛沙坦处理组 (组 2 )、血管紧张素Ⅱ和PD12 3319处理组 (组 3)。检测核增殖抗原表达、细胞数目及一氧化氮合酶含量的变化。结果 :组 2细胞数目为 ( 4 .17± 0 .15 )× 10 5个 ,核增殖抗原平均光密度为 0 .2 0 2 6± 0 .0 0 76 ,较组 3细胞明显减少 (P <0 .0 1) ;而组 2细胞一氧化氮合酶平均光密度为 0 .0 2 75±0 .0 0 2 1,明显高于组 3细胞 ( 0 .0 16 9± 0 .0 0 2 0 ) (P <0 .0 1)。结论 :血管紧张素Ⅱ可能通过其 2型受体表现为抑制血管平滑肌细胞增殖、拮抗 1型受体的作用 ,血管紧张素Ⅱ 2型受体的这种作用可能与增强一氧化氮合酶活性 ,使细胞合成、释放一氧化氮增多有关。Objective:To observe the affection of angiotensin Ⅱ antagonists on the cultured subtype 2 receptor of angiotensin II transfected aortic vascular smooth muscle cells of rat.Methods:After transfected the plasmid that contained the cDNA of subtype 2 receptor of angiotensin II into cultured rat vascular smooth muscle cells, the cells were divided into three groups:cells of group 1 were treated with angiotensinⅡ,cells of group 2 were treated with angiotensinⅡand losartan,cells of group 3 were treated with angiotensinⅡ and PD123319 .After experiments,the expression of PCNA, NOS and the cell number was tested, respectively.Results:After treated with Losartan,the cell number of group 2 was(4.17±0.15)×10 5,the OD value of PCNA was 0.202 6±0.007 6,both of which were less than that of cells of group 3;the OD value of NOS of cells was more in group 2(0.027 5±0.002 1 ) than that in group 3 (0.016 9±0.002 0) ( P <0.01).Conclusions:It suggests that when being activated,subtype 2 receptor of angiotensin Ⅱ could inhibit the proliferation of vascular smooth muscle cells and antagonist the effect of subtype 1 receptor of angiotensin Ⅱ,such an effect may be related to the activation of NOS.

关 键 词:血管紧张素Ⅱ 洛沙坦 PD123319 细胞增殖 一氧化氮合酶 

分 类 号:R972[医药卫生—药品] R965.2[医药卫生—药学]

 

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