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 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 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°. At the plateau, 20 mM L-NAME was 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 mean ± 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.