Sensory nerve-mediated and nitric oxide-dependent cutaneous vasodilation in normotensive and prehypertensive non-Hispanic blacks and whites.
Sensory nerve-mediated and nitric oxide-dependent cutaneous vasodilation in normotensive and prehypertensive non-Hispanic blacks and whites.
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血压正常和高血压前期的非西班牙裔黑人和白人中感觉神经介导的和一氧化氮依赖性的皮肤血管舒张。
DOI：
10.1152/ajpheart.00177.2020
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发表时间：
2020
期刊：
影响因子：
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通讯作者：
Quyyumi,ArshedA
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作者：
Wong,BrettJ;Turner,CaseyG;Miller,JamesT;Walker,DemetriaC;Sebeh,Yesser;Hayat,MatthewJ;Otis,JeffreyS;Quyyumi,ArshedA
本研究的目的是调查种族和亚临床血压升高（即高血压前期）对皮肤感觉神经介导和一氧化氮 (NO) 依赖性血管舒张的影响。我们招募了自认为是非西班牙裔黑人 (n= 16) 或非西班牙裔白人 (n= 16) 的参与者。在每组中，参与者被细分为血压正常（每组 n = 8 名）或高血压前期（每组 n = 8 名）。每个参与者都配备了四种皮内微透析纤维：1）对照（乳酸林格氏），2）5％利多卡因（感觉神经抑制），3）20 mMNω-硝基-l-精氨酸甲酯（l-NAME）（NO合酶抑制），和4）利多卡因+l-NAME。通过激光多普勒血流测定法评估皮肤血流量，每个部位均进行 33°C 至 39°C 的局部加热。在平台期，在对照和利多卡因位点输注 20 mMl-NAME 以量化 NO 依赖性血管舒张。通过 54 mM 硝普钠并局部加热至 43°C 诱导最大血管舒张。数据为平均值±SD。与血压正常的非西班牙裔白人 (54±12%) 相比，高血压前期非西班牙裔白人 (34±7%) 和两个非西班牙裔黑人组 (血压正常，20±±9%，高血压前期为 24±±15%) 感觉神经介导的皮肤血管舒张减少。与血压正常的非西班牙裔白人 (60±11%) 相比，高血压前期非西班牙裔白人 (41±±7%) 和两个非西班牙裔黑人组 (血压正常，44±±7%，高血压前期，19±±7%) 的 NO 依赖性血管舒张也有所减少。相对于所有其他群体，非西班牙裔黑人高血压前期的一氧化氮依赖性血管舒张功能的减少进一步减少。这些数据表明，亚临床血压升高会对非西班牙裔黑人和白人的感觉介导和一氧化氮依赖性血管舒张产生不利影响。新的和值得注意的已知显性高血压会减少皮肤感觉神经介导的和一氧化氮 (NO) 依赖性血管舒张，但亚临床血压升高（即高血压前期）的影响尚不清楚。种族和高血压前期的综合影响也是未知的。在这项研究中，我们发现，高血压前期可减少非西班牙裔白人和黑人群体中皮肤感觉神经介导的和一氧化氮依赖性血管舒张，其中在高血压前期非西班牙裔黑人中观察到的减少幅度最大。请收听本文相应的播客：https://ajpheart.podbean.com/e/race-blood-Pressure-and-microangio-function/。
The purpose of this study was to investigate the effect of race and subclinical elevations in blood pressure (i.e., prehypertension) on cutaneous sensory nerve-mediated and nitric oxide (NO)-dependent vasodilation. We recruited participants who self-identified as either non-Hispanic black (n= 16) or non-Hispanic white (n= 16). Within each group, participants were subdivided as either normotensive (n= 8 per group) or prehypertensive (n= 8 per group). Each participant was instrumented with four intradermal microdialysis fibers:1) control (lactated Ringer’s),2) 5% lidocaine (sensory nerve inhibition),3) 20 mMNω-nitro-l-arginine methyl ester (l-NAME) (NO synthase inhibition), and4) lidocaine +l-NAME. Skin blood flow was assessed via laser-Doppler flowmetry, and each site underwent local heating from 33°C to 39°C. At the plateau, 20 mMl-NAME were infused at control and lidocaine sites to quantify NO-dependent vasodilation. Maximal vasodilation was induced via 54 mM sodium nitroprusside and local heating to 43°C. Data are means ± SD. Sensory nerve-mediated cutaneous vasodilation was reduced in prehypertensive non-Hispanic white (34 ± 7%) and both non-Hispanic black groups (normotensive, 20 ± 9%, prehypertensive, 24 ± 15%) relative to normotensive non-Hispanic whites (54 ± 12%). NO-dependent vasodilation was also reduced in prehypertensive non-Hispanic white (41 ± 7%) and both non-Hispanic black groups (normotensive, 44 ± 7%, prehypertensive, 19 ± 7%) relative to normotensive non-Hispanic whites (60 ± 11%). The decrease in NO-dependent vasodilation in prehypertensive non-Hispanic blacks was further reduced relative to all other groups. These data suggest subclinical increases in blood pressure adversely affect sensory-mediated and NO-dependent vasodilation in both non-Hispanic blacks and whites.NEW & NOTEWORTHYOvert hypertension is known to reduce cutaneous sensory nerve-mediated and nitric oxide (NO)-dependent vasodilation, but the effect of subclinical increases in blood pressure (i.e., prehypertension) is unknown. The combined effect of race and prehypertension is also unknown. In this study, we found that prehypertension reduces cutaneous sensory nerve-mediated and NO-dependent vasodilation in both non-Hispanic white and black populations, with the greatest reductions observed in prehypertensive non-Hispanic blacks.Listen to this article's corresponding podcast at https://ajpheart.podbean.com/e/race-blood-pressure-and-microvascular-function/.