Nitric oxide (NO)-mediated endothelial dysfunction, secondary to increased oxidative stress, presents in young African American (AA) compared to European American (EA) adults, and may be modulated by vitamin D status. We assessed cutaneous microvascular function in 18 young, healthy (21±2 yr; 9 M, 9 F) subjects before (pre: 8 AA, 10 EA) and 13 subjects after (post: 7 AA, 6 EA) four weeks of 2,000 IU/day oral vitamin D supplementation. Serum vitamin D concentrations [25(OH)D] were measured at each visit. Three intradermal microdialysis fibers placed in the ventral forearm were randomized for treatment with 10 μM tempol, 100 μM apocynin, or lactated Ringer's (control). Local heating (39˚C) induced cutaneous vasodilation; red cell flux was measured at each site (laser-Doppler flowmetry) and cutaneous vascular conductance (CVC=flux/MAP) was expressed as a percentage of maximum (28mM sodium nitroprusside+43°C) for each phase of the local heating response. After attaining stable elevated blood flow, 15mM N^G-nitro-L-arginine methyl ester (L-NAME; NO synthase inhibitor) was perfused at all sites to quantify the NO contribution to cutaneous vasodilation (%NO), calculated as the difference between local heating and L-NAME plateaus. Serum [25(OH)D], the magnitude of the local heating response, and %NO were all lower in AA versus EA (p<0.01). Tempol (p=0.01), but not apocynin (p≥0.19), improved the local heating response and %NO. Four weeks of supplementation improved serum [25(OH)D], the local heating response, and %NO in AA (p≤0.04), but not EA (p≥0.41). Vitamin D supplementation mitigated endothelial dysfunction, an antecedent to overt CVD, in otherwise healthy, young AA adults.

中文翻译：

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4 周的维生素 D 补充剂可改善大学生非裔美国人的一氧化氮介导的微血管功能。

与欧洲美国人 (EA) 成人相比，一氧化氮 (NO) 介导的内皮功能障碍继发于氧化应激增加，出现在年轻的非洲裔美国人 (AA) 中，并且可能受维生素 D 状态的调节。我们评估了 18 名年轻、健康（21±2 岁；9 M、9 F）受试者的皮肤微血管功能，之前（前：8 AA，10 EA）和 13 名受试者之后（后：7 AA，6 EA）2,000 IU/天口服维生素 D 补充剂。在每次访问时测量血清维生素 D 浓度 [25(OH)D]。放置在前臂腹侧的三个皮内微透析纤维随机使用 10 μM tempol、100 μM 夹竹桃素或乳酸林格氏液（对照）进行治疗。局部加热 (39˚C) 引起皮肤血管舒张；在每个部位测量红细胞流量（激光多普勒血流仪），皮肤血管电导（CVC=flux/MAP）表示为局部加热反应每个阶段的最大值（28mM 硝普钠 + 43°C）的百分比。达到稳定升高的血流量后，15mM N^G-硝基-L-精氨酸甲酯（L-NAME；NO 合酶抑制剂）在所有部位灌注以量化 NO 对皮肤血管舒张的贡献 (%NO)，计算为局部加热和 L-NAME 平台之间的差异。AA 中的血清 [25(OH)D]、局部加热响应的幅度和 %NO 均低于 EA（p<0.01）。Tempol (p=0.01)，但不是夹竹桃素 (p≥0.19)，改善了局部加热响应和 %NO。4 周的补充改善了血清 [25(OH)D]、局部加热反应和 AA 中的 %NO (p≤0.04)，但没有改善 EA (p≥0.41)。补充维生素 D 减轻了内皮功能障碍，这是明显 CVD 的前因，在其他健康的年轻 AA 成年人中。