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首页> 外文期刊>Kidney Research and Clinical Practice >Effects of oxidative stress on endothelial modulation of contractions in aorta from renal hypertensive rats
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Effects of oxidative stress on endothelial modulation of contractions in aorta from renal hypertensive rats

机译：氧化应激对肾性高血压大鼠主动脉内皮细胞收缩调节的影响

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Background: Endothelial dysfunction is linked to exaggerated production of superoxide anions. This study was conducted to examine the effects of oxidative stress on endothelial modulation of contractions in chronic two-kidney, one-clip (2K1C) renal hypertensive rats. Methods: The 2K1C hypertension was induced by clipping the left renal artery; age-matched rats receiving sham treatment served as controls. Thoracic aortae were isolated and mounted in tissue baths for measurement of isometric tension. Results: Norepinephrine-induced contraction was augmented by the removal of the endothelium, which was more pronounced in sham rats than in 2K1C rats. N@w-nitro-L-arginine methyl ester, an inhibitor of nitric oxide production, had a similar augmenting effect. Vitamin C inhibited the contraction in aortic rings with intact endothelium from 2K1C rats but not from sham rats. The contraction was also suppressed by treatment with diphenyleneiodonium or apocynin, inhibitors of nicotinamide adenine dinucleotideicotinamide adenine dinucleotide phosphate (NADH/NADPH) oxidase, in the aortae with intact endothelium from 2K1C rats but not in those from sham rats. Superoxide anions generated by xanthine oxidase/hypoxanthine enhanced the contraction in the aortae with intact endothelium from sham rats, but had no effect in 2K1C rats. Enhanced contractile responses to norepinephrine by xanthine oxidase/hypoxanthine in sham rats were reversed by vitamin C. Conclusion: These results suggest that the effect on endothelial modulation of endothelium-derived nitric oxide is impaired in 2K1C hypertension. The impairment is, at least in part, related to increased production of superoxide anions by NADH/NADPH oxidase.
机译：背景：内皮功能障碍与超氧化物阴离子的过度产生有关。进行了这项研究以检查氧化应激对慢性二肾一夹（2K1C）肾性高血压大鼠的内皮细胞收缩调节的影响。方法：2K1C高血压是通过钳制左肾动脉而引起的。接受假手术的年龄匹配的大鼠作为对照。分离胸主动脉并将其安装在组织浴中以测量等轴测张力。结果：去甲肾上腺素诱导的收缩通过去除内皮而增强，在假手术大鼠中比在2K1C大鼠中更明显。一氧化氮产生的抑制剂N-w-硝基-L-精氨酸甲酯具有类似的增强作用。维生素C抑制2K1C大鼠完整血管内皮的收缩，但不抑制假大鼠的血管收缩。在带有完整内皮的2K1C大鼠的主动脉中用烟酰胺腺嘌呤二核苷酸/烟酰胺腺嘌呤二核苷酸磷酸酯（NADH / NADPH）氧化酶抑制剂二苯撑碘铵或载脂蛋白处理，也可抑制收缩，而2K1C大鼠则具有完整的内皮。黄嘌呤氧化酶/次黄嘌呤产生的超氧阴离子可增强假手术大鼠内皮完整的主动脉收缩，但在2K1C大鼠中无作用。黄嘌呤氧化酶/次黄嘌呤在假手术大鼠中对去甲肾上腺素的增强收缩反应被维生素C逆转。结论：这些结果表明，在2K1C高血压中，内皮对一氧化氮的内皮调节作用受到损害。该损伤至少部分地与NADH / NADPH氧化酶产生的超氧阴离子的增加有关。

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