Gene transfer of endothelial nitric oxide synthase reduces angiotensin II-Induced endothelial dysfunction
Gene transfer of endothelial nitric oxide synthase reduces angiotensin II-Induced endothelial dysfunction
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DOI：
10.1161/01.hyp.35.2.595
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发表时间：
2000-02-01
期刊：
影响因子：
8.3
通讯作者：
Heistad, DD
中科院分区：
文献类型：
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作者：
Nakane, H;Miller, FJ;Heistad, DD
血管紧张素 II 刺激血管 NADPH 氧化酶产生超氧化物，超氧化物可与一氧化氮发生反应，损害血管舒缩功能。我们测试了内皮一氧化氮合酶 (eNOS) 或超氧化物歧化酶 (SOD) 的过度表达将纠正血管紧张素 II 诱导的内皮功能障碍的假设。我们检查了将 eNOS 或 2 种 SOD 亚型基因转移至经血管紧张素 II 治疗的兔子主动脉后对血管舒缩功能的影响。通过微型渗透泵用血管紧张素II (100 ng·kg(-1)·min(-1))或盐水治疗新西兰白兔1周。在接受血管紧张素 II 治疗的兔子中，平均血压为 107+/-8 mm Hg；在注射生理盐水的兔子中，该值是 67+/-5 mm Hg（P
Angiotensin II stimulates vascular NADPH oxidase to produce superoxide, which can react with nitric oxide and impair vasomotor function. We tested the hypothesis that the overexpression of endothelial nitric oxide synthase (eNOS) or superoxide dismutase (SOD) would correct angiotensin II-induced endothelial dysfunction. We examined the effects of the gene transfer of eNOS or 2 isoforms of SOD to the aorta in angiotensin II-treated rabbits on vasomotor function. New Zealand White rabbits were treated for 1 week with angiotensin II (100 ng . kg(-1) . min(-1)) or saline by osmotic minipumps. In angiotensin II-treated rabbits, mean blood pressure was 107+/-8 mm Hg; it was 67+/-5 mm Hg in saline-infused rabbits (P