NO effect produced by UVA irradiation of skin is independent of NOS and temperature

Abstract

Ultraviolet-A (UVA) is known to induce nitrite photolysis, forming nitric oxide (NO). Recent studies have shown that UVA irradiation of human subjects reduces blood pressure and generates increased circulating nitrogen oxides. These may arise from nitrite/nitrate photolysis or from de novo synthesis by nitric oxide synthase enzymes. We wished to identify the source of this NO rise, and measure the extent of UVA induced vasorelaxation. Twelve healthy male volunteers (22 ± 1 years) underwent venous occlusion plethysmography to measure forearm blood flow (FBF). Volunteers attended on two occasions for sham (temperature control) or active forearm UVA irradiation (20 J/cm 2 ). NO production was blocked by intrabrachial artery infusion of the NO synthase inhibitor, L-NMMA (8 μmol/min), on both visits. Skin temperature was constantly monitored and controlled using an electric fan. Blood samples were drawn from both the irradiated arm and the contralateral arm for blood nitro-species analysis. Local skin temperature was similar between sham and active irradiation visits (change from baseline <0.5 °C, P = 0.9112). In the presence of local NO synthase inhibition, local UVA irradiation increased FBF (maximal increase 23.7 ± 6.5%, P < 0.05) for at least 30 min. In contrast, there was no significant change in blood flow after sham irradiation. Blood nitrite concentrations appear to rise after active irradiation but not after sham, however this did not achieve statistical significance. UVA irradiation of human skin evokes NOS and temperature independent vasodilatation. This effect is probably due to photolysis of pre-formed skin and circulatory stores of nitrogen oxides.