Acute ultraviolet radiation exposure attenuates nitric oxide-mediated vasodilation in the cutaneous microvasculature of healthy humans

S. Tony Wolf, Anna E. Stanhewicz, Nina G. Jablonski, W. Larry Kenney

Research output: Contribution to journalArticle

2 Citations (Scopus)

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 UVBexposed (300 mJ/cm2), 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 NG-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 NOmediated vasodilatio.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 UVBexposed 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.

Original languageEnglish (US)
Pages (from-to)1232-1237
Number of pages6
JournalJournal of applied physiology
Volume125
Issue number4
DOIs
StatePublished - Oct 2018

Fingerprint

Microvessels
Vasodilation
Nitric Oxide
Skin
Skin Pigmentation
Laser-Doppler Flowmetry
Arm
Reactive Oxygen Species
Radiation Exposure
5-methyltetrahydrofolate
NG-Nitroarginine Methyl Ester
Melanins
Microdialysis
Nitroprusside
Forearm
Nitric Oxide Synthase
Heating
Biological Availability
Blood Vessels
Young Adult

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

Cite this

@article{f47b03cceb9e4b72a3ac62ab7e02418e,
title = "Acute ultraviolet radiation exposure attenuates nitric oxide-mediated vasodilation in the cutaneous microvasculature of healthy humans",
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 UVBexposed (300 mJ/cm2), 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 NG-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 NOmediated vasodilatio.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 UVBexposed 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.",
author = "Wolf, {S. Tony} and Stanhewicz, {Anna E.} and Jablonski, {Nina G.} and Kenney, {W. Larry}",
year = "2018",
month = "10",
doi = "10.1152/japplphysiol.00501.2018",
language = "English (US)",
volume = "125",
pages = "1232--1237",
journal = "Journal of Applied Physiology",
issn = "8750-7587",
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}

Acute ultraviolet radiation exposure attenuates nitric oxide-mediated vasodilation in the cutaneous microvasculature of healthy humans. / Wolf, S. Tony; Stanhewicz, Anna E.; Jablonski, Nina G.; Kenney, W. Larry.

In: Journal of applied physiology, Vol. 125, No. 4, 10.2018, p. 1232-1237.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Acute ultraviolet radiation exposure attenuates nitric oxide-mediated vasodilation in the cutaneous microvasculature of healthy humans

AU - Wolf, S. Tony

AU - Stanhewicz, Anna E.

AU - Jablonski, Nina G.

AU - Kenney, W. Larry

PY - 2018/10

Y1 - 2018/10

N2 - 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 UVBexposed (300 mJ/cm2), 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 NG-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 NOmediated vasodilatio.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 UVBexposed 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.

AB - 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 UVBexposed (300 mJ/cm2), 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 NG-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 NOmediated vasodilatio.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 UVBexposed 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.

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