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Endothelium derived nitric oxide (NO) regulates vascular tone and blood pressure in man. NO also inhibits platelet aggregation and mediates a variety of beneficial anti-inflammatory and repair mechanisms. NO may also be a mediator in the release of the endogenous fibrinolytic factor, tissue-plasminogen activating factor (t-PA) from the endothelium.1 Via these actions it plays a very important role in protection of the vasculature from atherothrombosis and clinical sequelae such as myocardial infarction and stroke.
Visible and ultraviolet (UV) light relax vascular smooth muscles by producing NO in a phenomenon known as photorelaxation.2 The investigators have demonstrated significant stores of pre-formed, bound NO and other nitrosospecies in human skin, which are rapidly released upon exposure to UVA.3 The investigators have demonstrated recently that serum nitrite and nitroso-species are increased after standing in a UVA phototherapy cabinet and that local UVA exposure is associated with increased forearm arterial blood flow that is independent of skin temperature. The investigators have also demonstrated a fall in mean arterial blood pressure in subjects exposed UVA.
Cardiovascular morbidity and the prevalence of hypertension vary with latitude. The investigators hypothesise that some of this geographical variation may be explained by a diminished sunlight/UVA exposure with attendant negative effects upon NO bio-availability.4 To further examine the potential beneficial effects of UVA exposure we will examine the effects of whole-body UVA upon platelet activation and upon myocardial/coronary arterial flow reserve. The investigators will correlate these measures with systemic nitrate, nitrite and nitroso-species content in healthy volunteers.
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