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首页> 外文期刊>American Journal of Physiology >Angiotensin II-induced hypertrophy is potentiated in mice overexpressing p22phox in vascular smooth muscle.
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Angiotensin II-induced hypertrophy is potentiated in mice overexpressing p22phox in vascular smooth muscle.

机译：在血管平滑肌中过表达p22phox的小鼠中，血管紧张素II诱导的肥大得到增强。

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Increased reactive oxygen species (ROS) are implicated in several vascular pathologies associated with vascular smooth muscle hypertrophy. In the current studies, we utilized transgenic (Tg) mice (Tg(p22smc)) that overexpress the p22(phox) subunit of NAD(P)H oxidase selectively in smooth muscle. These mice have a twofold increase in aortic p22(phox) expression and H(2)O(2) production and thus provide an excellent in vivo model in which to assess the effects of increased ROS generation on vascular smooth muscle cell (VSMC) function. We tested the hypothesis that overexpression of VSMC p22(phox) potentiates angiotensin II (ANG II)-induced vascular hypertrophy. Male Tg(p22smc) mice and negative littermate controls were infused with either ANG II or saline for 13 days. Baseline blood pressure was not different between control and Tg(p22smc) mice. ANG II significantly increased blood pressure in both groups, with this increase being slightly exacerbated in the Tg(p22smc) mice. Baseline aortic wall thicknessand cross-sectional wall area were not different between control and Tg(p22smc) mice. Importantly, the ANG II-induced increase in both parameters was significantly greater in the Tg(p22smc) mice compared with control mice. To confirm that this potentiation of vascular hypertrophy was due to increased ROS levels, additional groups of mice were coinfused with ebselen. This treatment prevented the exacerbation of hypertrophy in Tg(p22smc) mice receiving ANG II. These data suggest that although increased availability of NAD(P)H oxidase-derived ROS is not a sufficient stimulus for hypertrophy, it does potentiate ANG II-induced vascular hypertrophy, making ROS an excellent target for intervention aimed at reducing medial thickening in vivo.
机译：活性氧增加（ROS）参与与血管平滑肌肥大相关的几种血管病变。在当前的研究中，我们利用了在平滑肌中选择性过表达NAD（P）H氧化酶的p22（phox）亚基的转基因（Tg）小鼠（Tg（p22smc））。这些小鼠的主动脉p22（phox）表达和H（2）O（2）产量增加​​了两倍，因此提供了一个出色的体内模型，可用来评估ROS生成对血管平滑肌细胞（VSMC）功能的影响。我们测试了VSMC p22（phox）的过表达增强血管紧张素II（ANG II）诱导的血管肥大的假设。雄性Tg（p22smc）小鼠和同窝阴性对照组分别注射ANG II或生理盐水13天。对照组和Tg（p22smc）小鼠之间的基线血压没有差异。 ANG II均显着增加了两组的血压，这种升高在Tg（p22smc）小鼠中略有加重。对照和Tg（p22smc）小鼠之间的基线主动脉壁厚度和横截面积没有差异。重要的是，与对照小鼠相比，Tg（p22smc）小鼠中ANG II诱导的两个参数的增加都明显更大。为了确认这种血管肥大的增强是由于ROS水平升高所致，将额外的小鼠组与依布硒仑合用。这种治疗防止了接受ANG II的Tg（p22smc）小鼠中肥大的恶化。这些数据表明，尽管增加的NAD（P）H氧化酶来源的ROS的可用性不足以刺激肥大，但它确实增强了ANG II诱导的血管肥大，使ROS成为旨在减少体内内侧增厚的干预措施的出色靶标。

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