Endothelial function is dependent on the balance between vasoconstrictive and vasodilatory substances. The endothelium ability to produce nitric oxide is one of the most crucial mechanisms in regulating vascular tone. An increase in inducible nitric oxide synthase contributes to endothelial dysfunction in overweight persons, while oxidative stress contributes to the conversion of nitric oxide to peroxynitrite (measured as nitrotyrosine in vivo) in underweight persons. The objective of this study was to elucidate the interaction of body composition and oxidative stress on vascular function and peroxynitrite. This was done through an experimental design with three weight groups (underweight, normal weight and overweight), with four treatment arms in each. Plasma nitrotyrosine levels were measured 15–20 h post lipopolysaccharide (LPS) treatment, as were aortic ring tension changes. Acetylcholine (ACh) and sodium nitroprusside (SNP) challenges were used to observe endothelial-dependent and endothelial-independent vascular relaxation after pre-constriction of aortic rings with phenylephrine. Nitrotyrosine levels in saline-treated rats were similar among the weight groups. There was a significant increase in nitrotyrosine levels between saline-treated rats and those treated with the highest lipopolysaccharide doses in each of the weight groups. In response to ACh challenge, Rmax (percentage reduction in aortic tension) was lowest in overweight rats (112%). In response to SNP, there was an insignificantly lower Rmax in the underweight rats (106%) compared to the normal weight rats (112%). Overweight rats had a significant decrease in Rmax (83%) in response to SNP, signifying involvement of a more chronic process in tension reduction changes. A lower Rmax accompanied an increase in peroxynitrite after acetylcholine challenge in all weight groups. Endothelial dysfunction, observed as an impairment in the ability to reduce tension, is associated with increased plasma peroxynitrite levels across the spectrum of body mass. In higher-BMI rats, an additional role is played by vascular smooth muscle in the causation of endothelial dysfunction.

中文翻译：

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内皮功能障碍和体重指数：血浆过氧亚硝酸盐有作用吗？


内皮功能取决于血管收缩物质和血管舒张物质之间的平衡。内皮产生一氧化氮的能力是调节血管张力的最关键机制之一。诱导型一氧化氮合酶的增加会导致超重人群的内皮功能障碍，而氧化应激会导致体重不足的人将一氧化氮转化为过氧亚硝酸盐（体内以硝基酪氨酸测量）。本研究的目的是阐明身体成分和氧化应激对血管功能和过氧亚硝酸盐的相互作用。这是通过三个体重组（体重不足、体重正常和体重超重）的实验设计完成的，每个组有四个治疗组。脂多糖 (LPS) 治疗后 15-20 小时测量血浆硝基酪氨酸水平，以及主动脉环张力变化。使用乙酰胆碱（ACh）和硝普钠（SNP）激发来观察用去氧肾上腺素预收缩主动脉环后内皮依赖性和内皮非依赖性血管舒张。经盐水处理的大鼠的硝基酪氨酸水平在体重组中相似。在每个体重组中，经盐水治疗的大鼠和经最高脂多糖剂量治疗的大鼠之间的硝基酪氨酸水平显着增加。在应对乙酰胆碱挑战时，超重大鼠的 Rmax（主动脉张力降低百分比）最低（112%）。针对 SNP，体重不足的大鼠 (106%) 与正常体重的大鼠 (112%) 相比，Rmax 略有降低。超重大鼠对 SNP 的反应 Rmax 显着降低 (83%)，这表明张力降低变化涉及更慢性的过程。 在所有体重组中，乙酰胆碱激发后，Rmax 降低，过氧亚硝酸盐增加。内皮功能障碍被观察为降低张力的能力受损，与体重范围内血浆过氧亚硝酸盐水平升高有关。在BMI较高的大鼠中，血管平滑肌在导致内皮功能障碍中发挥着额外的作用。