Contribution of sensory nerves to cutaneous reactive hyperaemia in non-Hispanic Black and White young adults.

NEW FINDINGS: What is the central question of this study? Does cutaneous sensory nerve-mediated vasodilatation differ between non-Hispanic Black and White young adults? What is the main finding and its importance? The magnitude of cutaneous reactive hyperaemia is lower in non-Hispanic Black relative to non-Hispanic White young adults, but the overall sensory nerve contribution is the same, suggesting that sensory nerve function is similar in both non-Hispanic Black and White young adults. ABSTRACT: The aim of this study was to assess cutaneous sensory nerve function, independent of nitric oxide, in non-Hispanic Black and White young adults. We tested the hypothesis that cutaneous reactive hyperaemia and sensory nerve-mediated vasodilatation would be lower in non-Hispanic Black young adults relative to non-Hispanic White young adults. Twenty-four participants who self-identified as non-Hispanic Black (n = 12) or non-Hispanic White (n = 12) were recruited. All participants underwent three bouts of reactive hyperaemia. An index of skin blood flow was measured continuously using laser-Doppler flowmetry at a control site and at a site treated with topical 4% lignocaine to inhibit sensory nerve function. Peak reactive hyperaemia was lower in non-Hispanic Black relative to non-Hispanic White participants (P < 0.001). Total reactive hyperaemia was lower in non-Hispanic Black [mean (SD); control, 4085 (955)%CVCmax  s; lignocaine, 2127 (639) percent maximal cutaneous vascular conductance * seconds, %CVCmax  s] relative to non-Hispanic White [control: 6820 (1179)%CVCmax  s; lignocaine, 3573 (712)%CVCmax  s] participants (P < 0.001 for both sites). There was no difference between groups for the calculated contribution of sensory nerves to either the peak [non-Hispanic Black, 25 (14)%; non-Hispanic White, 19 (13)%] or total reactive hyperaemic response [non-Hispanic Black, 48 (10)%; non-Hispanic White, 47 (10)%]. These data suggest that cutaneous reactive hyperaemia is lower in non-Hispanic Black young adults, but the sensory nerve contribution is similar in non-Hispanic Black and White young adults.

Sensory nerve-mediated and nitric oxide-dependent cutaneous vasodilation in normotensive and prehypertensive non-Hispanic blacks and whites.

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 mM Nω-nitro-l-arginine methyl ester (l-NAME) (NO synthase inhibition), and 4) 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 mM l-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 & NOTEWORTHY Overt 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.