Abstract
Nitric oxide (NO)‐dependent vasodilation is reduced in non‐Hispanic Blacks (NHB) compared to non‐Hispanic Whites (NHW), but it is not well‐established if this reduction is due to reduced endothelial‐dependent or endothelial‐independent vasodilation, or both. The purpose of this study was to examine endothelium‐dependent and endothelium‐independent mechanisms of cutaneous microvascular vasodilation between young, healthy NHB and NHW. Six participants who self‐identified as either NHB or NHW were instrumented with two microdialysis fibers in the skin of the forearm. A dose‐response was then completed at each site: 1) acetylcholine (ACh; 10−10– 10−1M) to assess endothelial‐dependent vasodilation, and 2) sodium nitroprusside (SNP; 10−10– 10−1M) to assess endothelial‐independent vasodilation. Each dose was perfused for 5 minutes. Local heaters were kept at 33°C throughout baseline and the dose‐response protocol. Maximal vasodilation was elicited by heating the skin to 43°C and infusing 54 mM SNP. Laser‐Doppler flowmetry (LDF) was used to assess an index of skin blood flow. Cutaneous vascular conductance (CVC) was calculated (LDF/MAP) and normalized to maximal blood flow (%CVCmax). Data are presented as mean ± standard deviation. The %CVCmax response to ACh in NHB was significantly reduced compared to NHW at all concentrations >10−4 M (10−3: NHB 20 ± 13 vs. NHW 66 ± 8 %CVCmax; 10−2: NHB 25 ± 3 vs. NHW 76 ± 8 %CVCmax; 10−1: NHB 39 ± 15 vs. NHW 84 ± 8 %CVCmax;P< 0.05 for all). The ACh log EC50 was higher for NHB (−1 ± 0.6 M) compared to NHW (−3.5 ± 0.8 M; P< 0.05). The %CVCmax response to SNP was similar between NHB and NHW for all concentrations tested. Similarly, there was no difference in log EC50 between NHB (−1.5 ± 0.6 M) and NHW (−2.1 ± 0.4 M). Reduced NO‐dependent vasodilation in NHB compared NHW appears to result from decreased endothelial‐dependent mechanisms, and not endothelial‐independent mechanisms. This information supports suggestions from previous research in the field and may aid in understanding the discrepancy in disease risk between NHB and NHW.
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