Role of superoxide anion in regulating pressor and vascular hypertrophic response to angiotensin II.
Role of superoxide anion in regulating pressor and vascular hypertrophic response to angiotensin II.
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DOI：
10.1152/ajpheart.00914.2001
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发表时间：
2002-05
期刊：
影响因子：
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通讯作者：
Hui Di Wang;D. Johns;Shanqin Xu;R. Cohen
中科院分区：
文献类型：
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作者：
Hui Di Wang;D. Johns;Shanqin Xu;R. Cohen
我们的目的是解决NAPDH氧化酶衍生的超氧阴离子在血管对ANG II的反应中的作用。比较了野生型小鼠和过表达人超氧化物歧化酶（hSOD）小鼠的血压、主动脉超氧阴离子、3-硝基酪氨酸和内侧横截面积。在hSOD小鼠中，angii的升压反应明显较弱。野生型小鼠的超氧阴离子水平增加了两倍，而hSOD小鼠则没有。3-硝基酪氨酸在野生型小鼠主动脉内皮和外膜中升高，而在hSOD小鼠中无升高。相比之下，hSOD小鼠的主动脉内侧横截面积增加了50%，与野生型小鼠相当。表达hSOD的小鼠对ANG II的降压反应较低，这与野生型小鼠中超氧阴离子的降压作用一致，很可能是因为它与一氧化氮发生反应。尽管阻止了超氧阴离子和3-硝基酪氨酸的增加，但体内主动脉对ANG II的肥厚反应不受hSOD的影响。
Our purpose was to address the role of NAPDH oxidase-derived superoxide anion in the vascular response to ANG II. Blood pressure, aortic superoxide anion, 3-nitrotyrosine, and medial cross-sectional area were compared in wild-type mice and in mice that overexpress human superoxide dismutase (hSOD). The pressor response to ANG II was significantly less in hSOD mice. Superoxide anion levels were increased twofold in ANG II-treated wild-type mice but not in hSOD mice. 3-Nitrotyrosine increased in aortic endothelium and adventitia in wild-type but not hSOD mice. In contrast, aortic medial cross-sectional area increased 50% with ANG II in hSOD mice, comparable to wild-type mice. The lower pressor response to ANG II in the mice expressing hSOD is consistent with a pressor role of superoxide anion in wild-type mice, most likely because it reacts with nitric oxide. Despite preventing the increase in superoxide anion and 3-nitrotyrosine, the aortic hypertrophic response to ANG II in vivo was unaffected by hSOD.