Journal article
Acute ultraviolet radiation exposure attenuates nitric oxide-mediated vasodilation in the cutaneous microvasculature of healthy humans
Journal of applied physiology (1985), Vol.125(4), pp.1232-1237
08/23/2018
DOI: 10.1152/japplphysiol.00501.2018
PMCID: PMC6230571
PMID: 30138076
Abstract
5-Methyltetrahydrofolate (5-MTHF) is important for nitric oxide (NO)-mediated cutaneous microvascular vasodilation. Ultraviolet B (UVB) radiation may deplete 5-MTHF, either directly or via production of reactive oxygen species (ROS), decreasing NO-mediated vasodilation. We hypothesized that
1)
acute UVB exposure would attenuate NO-dependent cutaneous vasodilation,
2)
local perfusion of 5-MTHF or ascorbate (ASC) (antioxidant) would augment NO-dependent vasodilation after UVB, and
3)
darker skin pigmentation would be UVB-protective. Intradermal microdialysis fibers (
n
= 3) placed in each forearm of 22 healthy young adults (23 ± 1 yr; 8M/14F) locally delivered lactated Ringer’s (control), 5 mM 5-MTHF, or 10 mM ASC. One arm was UVB-exposed (300 mJ/cm
2
), and the other served as a nonexposed control (CON). Following UVB exposure, a standardized local heating (42°C) protocol induced cutaneous vasodilation. After attaining a plateau blood flow, 15 mM N
G
-nitro-
l
-arginine methyl ester (nitric oxide synthase inhibiter) was infused at all sites to quantify the NO contribution. Red cell flux was measured at each site by laser-Doppler flowmetry (LDF), and cutaneous vascular conductance (CVC = LDF/mean arterial pressure) was expressed as a percentage of maximum (28 mM sodium nitroprusside + 43°C). UVB attenuated NO-mediated vasodilation compared with CON (23.1 ± 3.6 vs. 33.9 ± 3.4%;
P
= 0.001). Delivery of 5-MTHF or ASC improved NO-mediated vasodilation versus lactated Ringer’s in the UVB-exposed arm (MTHF: 30.1 ± 4.8% vs. 23.1 ± 3.8%;
P
= 0.03; ASC: 30.9 ± 4.3% vs. 23.1 ± 3.8%;
P
= 0.02). Neither treatment affected the response in the nonexposed arm (
P
≥ 0.09). Skin pigmentation (melanin index) was not predictive of the UVB response (
P
≥ 0.34). These data suggest that acute UVB exposure attenuates NO-mediated vasodilation via direct and/or ROS-induced reductions in 5-MTHF, independent of skin pigmentation.
NEW & NOTEWORTHY
Endothelial-derived nitric oxide (NO) contributes to normal healthy function of the human cutaneous microvasculature. Bioavailability of 5-methyltetrahydrofolate (5-MTHF) is important for the production of NO. Ultraviolet (UV) radiation exposure, specifically UVB, may deplete cutaneous 5-MTHF, thereby reducing NO-mediated microvascular function. Our findings suggest that acute UVB exposure attenuates NO-mediated vasodilation of the cutaneous microvasculature via degradation of 5-MTHF. These findings advance our understanding of the potential negative health impacts of acute UV exposure.
Details
- Title: Subtitle
- Acute ultraviolet radiation exposure attenuates nitric oxide-mediated vasodilation in the cutaneous microvasculature of healthy humans
- Creators
- S. Tony Wolf - Pennsylvania State UniversityAnna E Stanhewicz - Pennsylvania State UniversityNina G Jablonski - Pennsylvania State UniversityW. Larry Kenney - Pennsylvania State University
- Resource Type
- Journal article
- Publication Details
- Journal of applied physiology (1985), Vol.125(4), pp.1232-1237
- Publisher
- American Physiological Society
- DOI
- 10.1152/japplphysiol.00501.2018
- PMID
- 30138076
- PMCID
- PMC6230571
- ISSN
- 8750-7587
- eISSN
- 1522-1601
- Alternative title
- UV AND SKIN MICROVASCULAR FUNCTION
- Language
- English
- Date published
- 08/23/2018
- Academic Unit
- Fraternal Order of Eagles Diabetes Research Center; Health and Human Physiology; Internal Medicine
- Record Identifier
- 9984259650702771
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