title: Altered skin flowmotion in hypertensive humans.
abstract: Essential hypertensive humans exhibit attenuated cutaneous nitric oxide (NO)-dependent vasodilation. Using spectral analysis (fast Fourier transformation) we aimed to characterize the skin flowmotion contained in the laser-Doppler flowmetry recordings during local heating-induced vasodilation before and after concurrent pharmacological inhibition of nitric oxide synthase (NOS) in hypertensive and age-matched normotensive men and women. We hypothesized that hypertensive subjects would have lower total power spectral densities (PSDs), specifically in the frequency intervals associated with intrinsic endothelial and neurogenic control of the microvasculature. Furthermore, we hypothesized that NOS inhibition would attenuate the endothelial frequency interval. Laser-Doppler flowmetry recordings during local heating experiments from 18 hypertensive (MAP: 108±2mmHg) and 18 normotensive (MAP: 88±2mmHg) men and women were analyzed. Within site NO-dependent vasodilation was assessed by perfusion of a non-specific NOS inhibitor (N(G)-nitro-l-arginine methyl ester; l-NAME) through intradermal microdialysis during the heating-induced plateau in skin blood flow. Local heating-induced vasodilation increased total PSD for all frequency intervals (all p<0.001). Hypertensives had a lower total PSD (p=0.03) and absolute neurogenic frequency intervals (p<0.01) compared to the normotensives. When normalized as a percentage of total PSD, hypertensives had reduced neurogenic (p<0.001) and augmented myogenic contributions (p=0.04) to the total spectrum. NOS inhibition decreased total PSD (p<0.001) for both groups, but hypertensives exhibited lower absolute endothelial (p<0.01), neurogenic (p<0.05), and total PSD (p<0.001) frequency intervals compared to normotensives. These data suggest that essential hypertension results in altered neurogenic and NOS-dependent control of skin flowmotion and support the use of spectral analysis as a non-invasive technique to study vasoreactivity.
authors.affiliation: Department of Kinesiology, The Pennsylvania State University, University Park, PA 16802-6900, USA.
authors.forename: R S
authors.initials: RS
authors.lastname: Bruning
authors.affiliation: Department of Kinesiology, The Pennsylvania State University, University Park, PA 16802-6900, USA.
authors.forename: W L
authors.initials: WL
authors.lastname: Kenney
authors.affiliation: Department of Kinesiology, The Pennsylvania State University, University Park, PA 16802-6900, USA. Electronic address: lma191@psu.edu.
authors.forename: L M
authors.initials: LM
authors.lastname: Alexander
mesh_terms: D000279:Administration, Cutaneous; D062186:Arterial Pressure; D001783:Blood Flow Velocity; D016022:Case-Control Studies; D004791:Enzyme Inhibitors / Q000008:administration & dosage; D005260:Female; D005583:Fourier Analysis; D006361:Heating; D006358:Hot Temperature; D006801:Humans; D006973:Hypertension / Q000201:enzymology / Q000503:physiopathology*; D017078:Laser-Doppler Flowmetry; D008297:Male; D017551:Microdialysis; D008875:Middle Aged; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D012039:Regional Blood Flow; D012867:Skin / Q000098:blood supply*; D013997:Time Factors; D014664:Vasodilation; D014666:Vasomotor System / Q000503:physiopathology
chemical_list: D004791:Enzyme Inhibitors; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase