Department of Kinesiology, The Pennsylvania State University, University Park, Pennsylvania, United States.
Graduate Program in Physiology, The Pennsylvania State University, University Park, Pennsylvania, United States.
J Appl Physiol (1985). 2023 Jun 1;134(6):1403-1408. doi: 10.1152/japplphysiol.00118.2023. Epub 2023 Apr 20.
Ultraviolet radiation (UVR) exposure acutely reduces nitric oxide (NO)-dependent cutaneous vasodilation. In addition, increased constitutive skin melanin is associated with attenuated NO-dependent cutaneous vasodilation. However, the impact of within-limb variation in skin melanization, associated with seasonal UVR exposure, on NO-dependent cutaneous vasodilation is unknown. We investigated the effect of within-limb variation in skin melanin on NO-dependent cutaneous vasodilation. Intradermal microdialysis fibers were placed in the inner-upper arm, ventral forearm, and dorsal forearm of seven adults (33 ± 14 yr; 4 M/3 F) with constitutively light skin pigmentation. Melanin-index (M-index; an index of skin pigmentation), measured via reflectance spectrophotometry, confirmed differences in sun exposure among sites. A standardized local heating (42°C) protocol induced cutaneous vasodilation. After attaining a stable elevated blood flow plateau, 15 mM -nitro-l-arginine methyl ester (l-NAME; NO synthase inhibitor) was infused to quantify the NO contribution. Laser-Doppler flowmetry (LDF) measured red cell flux and cutaneous vascular conductance (CVC = LDF/mean arterial pressure) and was normalized to maximal (%CVC; 28 mM sodium nitroprusside + 43°C local heating). Dorsal forearm M-index was higher [50.5 ± 11.8 au (arbitrary units)] compared with the ventral forearm (37.5 ± 7.4 au; ≤ 0.03) and upper arm (30.0 ± 4.0 au; ≤ 0.001) M-index. Cutaneous vasodilation responses to local heating were not different among sites ( ≥ 0.12). Importantly, neither the magnitude of the local heating plateau (dorsal: 85 ± 21%; ventral: 70 ± 21%; upper: 87 ± 15%; ≥ 0.16) nor the NO-mediated component of that response (dorsal: 59 ± 15%; ventral: 54 ± 13%; upper: 55 ± 11%; ≥ 0.79) was different among sites. These data suggest that within-limb differences in skin pigmentation secondary to seasonal UVR exposure do not alter NO-dependent cutaneous vasodilation. Locally derived endothelial nitric oxide (NO) contributes to the full expression of cutaneous vasodilation responses. Acute ultraviolet radiation (UVR) exposure attenuates NO-mediated vasodilation of the cutaneous microvasculature. Our findings suggest that in constitutively lightly pigmented skin, variation in skin melanin due to seasonal exposure to UVR does not alter the NO contribution to cutaneous vasodilation. Seasonal UVR exposure does not impact the NO-mediated cutaneous microvascular function.
紫外线(UVR)辐射会急性降低依赖于一氧化氮(NO)的皮肤血管舒张。此外,皮肤中固有黑色素的增加与依赖于 NO 的皮肤血管舒张减弱有关。然而,与季节性 UVR 暴露相关的肢体内部皮肤色素沉着的变化对依赖于 NO 的皮肤血管舒张的影响尚不清楚。我们研究了肢体内部皮肤黑色素变化对依赖于 NO 的皮肤血管舒张的影响。在七个具有固有浅色皮肤色素沉着的成年人(33 ± 14 岁;4 男/3 女)的内上臂、前臂腹侧和前臂背侧放置了皮内微透析纤维。通过反射分光光度法测量黑色素指数(M-index;皮肤色素沉着的指标),以确认各部位之间的日晒差异。采用标准化局部加热(42°C)方案诱导皮肤血管舒张。在达到稳定的升高血流平台后,输注 15 mM -硝基-L-精氨酸甲酯(l-NAME;一氧化氮合酶抑制剂)以量化 NO 的贡献。激光多普勒流量测定法(LDF)测量红细胞通量和皮肤血管传导率(CVC=LDF/平均动脉压),并归一化为最大(%CVC;28 mM 硝普钠+43°C 局部加热)。与前臂(37.5 ± 7.4 au; ≤ 0.03)和上臂(30.0 ± 4.0 au; ≤ 0.001)相比,前臂背侧的 M-index 更高[50.5 ± 11.8 au(任意单位)]。局部加热引起的皮肤血管舒张反应在各部位之间没有差异( ≥ 0.12)。重要的是,局部加热平台的幅度(背侧:85 ± 21%;腹侧:70 ± 21%;上臂:87 ± 15%; ≥ 0.16)以及该反应的 NO 介导部分(背侧:59 ± 15%;腹侧:54 ± 13%;上臂:55 ± 11%; ≥ 0.79)在各部位之间均无差异。这些数据表明,由于季节性 UVR 暴露导致的肢体内部皮肤色素沉着差异不会改变依赖于 NO 的皮肤血管舒张。局部产生的内皮一氧化氮(NO)有助于皮肤血管舒张反应的完全表达。急性紫外线(UVR)辐射会减弱皮肤微血管的依赖于 NO 的血管舒张。我们的发现表明,在固有浅色色素沉着的皮肤中,由于季节性 UVR 暴露导致的皮肤黑色素变化不会改变 NO 对皮肤血管舒张的贡献。季节性 UVR 暴露不会影响依赖于 NO 的皮肤微血管功能。