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首页> 外文期刊>Stroke: A Journal of Cerebral Circulation >Angiotensin II produces superoxide-mediated impairment of endothelial function in cerebral arterioles.
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Angiotensin II produces superoxide-mediated impairment of endothelial function in cerebral arterioles.

机译：血管紧张素II在脑小动脉中产生超氧化物介导的内皮功能损害。

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BACKGROUND AND PURPOSE: Angiotensin II (Ang II) produces oxidative stress in vascular cells in culture and in extracranial conduit arteries. The goal of this study was to examine the hypothesis that Ang II produces superoxide-mediated impairment of endothelial function in cerebral microvessels. METHODS: Diameter of cerebral arterioles (baseline diameter=104+/-3 microm) was measured with the use of a closed cranial window in anesthetized rabbits. Topical application of Ang II was used to avoid effects on arterial pressure. RESULTS: Ang II (0.1 to 1 micromol/L for 2 hours) had no effect on baseline diameter (change in diameter of -3+/-2% in response to 1 micromol/L Ang II) but produced concentration-dependent inhibition of vasodilatation to the endothelium-dependent agonist bradykinin. For example, 1 micromol/L Ang II inhibited responses to 1 nmol/L bradykinin by almost 80%. These inhibitory effects of Ang II were prevented by the superoxide scavenger 4,5-dihydroxy-1,3-benzene-disulfonic acid (Tiron; 10 mmol/L) or diphenylene iodonium (DPI; 3 micromol/L), an inhibitor of NAD(P)H oxidase. Ang II did not inhibit vasodilatation in response to nitroprusside, an endothelium-independent vasodilator. CONCLUSIONS: These findings are the first evidence that local Ang II produces superoxide-mediated vascular dysfunction in cerebral microvessels. The results with DPI suggest that the source of superoxide may be an NAD(P)H oxidase.
机译：背景与目的：血管紧张素II（Ang II）在培养的血管细胞和颅外导管中产生氧化应激。这项研究的目的是检查Ang II产生超微介导的脑微血管内皮功能损害的假说。方法：使用封闭的颅窗测量麻醉兔子的脑小动脉直径（基线直径= 104 +/- 3微米）。局部应用Ang II可以避免对动脉压的影响。结果：Ang II（0.1至1 micromol / L，持续2小时）对基线直径没有影响（响应1 micromol / L Ang II，直径变化为-3 +/- 2％），但是对浓度的抑制作用取决于浓度血管舒张至内皮依赖性激动剂缓激肽。例如，1微摩尔/升的Ang II将对1 nmol / L缓激肽的反应抑制了近80％。 Ang II的这些抑制作用可通过超氧化物清除剂4,5-二羟基-1,3-苯二磺酸（Tiron; 10 mmol / L）或NAD抑制剂二亚苯基碘鎓（DPI; 3 micromol / L）来预防（P）H氧化酶。 Ang II不会抑制对内皮依赖性血管舒张剂硝普钠的血管舒张。结论：这些发现是局部Ang II在脑微血管中产生超氧化物介导的血管功能障碍的第一个证据。 DPI的结果表明，超氧化物的来源可能是NAD（P）H氧化酶。

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