Role of Angiotensin II in Injury‐Induced Neointima Formation in Rats
Role of Angiotensin II in Injury‐Induced Neointima Formation in Rats
复制标题
血管紧张素 II 在大鼠损伤诱导的新内膜形成中的作用
作者：
W. Osterrieder;Rita K.M. Miiller;J. Powell;J. Clozel;F. Hefti;H. Baumgartner
血管紧张素转换酶抑制剂显著抑制大鼠颈动脉球囊导管损伤后新生内膜的形成。为了确定这种作用是否通过血管活性肽血管紧张素II（Ang II）介导，遵循两种方法。首先，气球模型被用来比较连续输注的血管紧张素II的影响，有和没有同时转换酶抑制西拉普利;第二，口服活性的非肽类血管紧张素II受体拮抗剂DuP 753的影响进行了分析。在球囊损伤后14天进行形态测定分析。接受Ang II连续输注（0.3 μ/min/大鼠）的动物被发现对球囊损伤的反应比对照组有显著更大的新生内膜形成。用西拉普利（10 mg/kg/天）治疗的动物显著减少了新生内膜形成，但在接受血管紧张素II输注的动物中，用西拉普利治疗并不能抑制新生内膜病变的发展。在第二组实验中，DuP 753（10 mg/kg，每日两次）与西拉普利一样有效地防止新生内膜形成。这些数据支持的结论是，转换酶抑制剂通过抑制血管紧张素II的产生，防止血管损伤后的新生内膜形成。
Angiotensin converting enzyme inhibition markedly suppresses neointima formation in response to balloon catheter-induced vascular injury of the rat carotid artery. To determine whether this effect was mediated through the vasoactive peptide angiotensin II (Ang II), two approaches were followed. First, the balloon model was used to compare the effects of continuous infusion of Ang II, with and without concurrent converting enzyme inhibition by cilazapril; second, the effects of the orally active nonpeptidic Ang II receptor antagonist DuP 753 were analyzed. Morphometric analysis was performed at 14 days after balloon injury. Animals that received continuous infusion of Ang II (0.3 μ/min/rat) were found to have significantly greater neointima formation in response to balloon injury than controls. Animals treated with cilazapril (10 mg/kg/day) had markedly reduced neointima formation, but in animals receiving infusion of Ang II, treatment with cilazapril did not suppress development of neointimal lesions. In the second group of experiments, DuP 753 (10 mg/kg twice daily) was as effective to prevent neointima formation as cilazapril. These data sapport the conclusions that converting enzyme inhibition prevents neointima formation after vascular injury through inhibition of Ang II generation.
影响因子：
15.9
作者：
NAFTILAN, AJ;PRATT, RE;DZAU, VJ
通讯作者：
DZAU, VJ