OK, there seems to be something here. UV light releases nitric oxide from the skin. Who knew?

So, I’m starting some tanning today!

Here is some information from this link (the reference numbers can be found in the article from this link):

Beneficial Roles of UVA-induced Nitric Oxide (NO•) on Human Health
A few years ago it was demonstrated that nitric oxide (NO•), a gaseous free radical, is non-enzymatically induced in skin by UVA.128–130 However, UVA-induced NO• and its influence on human physiology and pathophysiology are not so well studied as the influence of NO• produced enzymatically by NO synthases.131 NO• is able to diffuse rapidly across cell membranes, and, depending on the conditions, is able to diffuse more than several hundred microns. The biological half-life of NO• is in the range from 1 ms to 2 sec, depending on superoxide (O2•-), antioxidants and oxygen concentrations.2 The biological effects of NO• are mediated through the reaction of NO• with a number of targets, such as haem groups, cysteine residues and iron and zinc clusters. This wide range of targets for NO• helps to explain the multiple roles it plays, including vasodilatation, immune defense, neurotransmission, regulation of cell death (apoptosis) and cell motility. Due to the importance of NO•, abnormal regulation of the concentration of UV-induced NO• may affect a number of important biological processes.
The rapid release of NO• following UVA exposure suggests the existence of latent stores. It is well known that part of the endogenously produced NO• is converted into nitrite (NO2-), nitrate or nitrosothiols. Earlier it was thought that these compounds are inert end products of endogenous NO• metabolism. In 2003 Rodriguez et al.132 demonstrated that in rat vascular tissue NO2- and nitrosothiols, but not nitrate, are converted back to NO• under UVA exposure

Protective effects of UV-induced NO•

Low concentrations of NO• protect cultured keratinocytes and skin from oxidative stress and UVA-induced apoptosis.130,131,134 The mechanism and the required concentrations for this protective action in skin are still unknown. Induction of Bcl-2 expression and inhibition of caspase activation have been suggested in some studies,130 but this fails to explain the rapid timescale of the response. It is possible that UVA-induced NO• may protect skin against solar radiation induced damages within 20–30 min, depending on UVA dose. Two independent studies have demonstrated that UVA exposure of human skin specimens leads to non-enzymatic NO• formation which reaches a maximum after 20 min (320–400 nm, 40 J/cm2) or after 30 min (350–400 nm, 30 J/cm2).128,133
In 2009 Oplander et al. demonstrated that irradiation of healthy individuals with biologically relevant doses of UVA lead to a sustained reduction in blood pressure.129 In 2010 it was proposed that many of the beneficial effects of sunlight related to cardiovascular health may be mediated by mechanisms that are independent of vitamin D and exposure to UV alone, but through UVA-induced NO• and nitrite.135 NO2-, for a long time considered biologically inert at low concentrations, is now known, not only to dilate blood vessels in its own right, but also to protect organs against ischemia/reperfusion damage.136 Hemoglobin, myoglobin, xanthine oxidoreductase, cytochrome P-450, and mitochondrial enzymes can all generate NO• from NO2- under hypoxic conditions.135,137 In adults, skin and blood are of comparable weight and volume. The total amount of NO2- in the epidermis is around 135 µM, while the total amount of NO2- in blood rarely exceeds 13–15 µM.133,135 Thus, mobilization of only a fraction of the relatively large epidermal pool of NO2- by sunlight is likely to be sufficient to increase plasma NO2- concentrations transiently. Thus, Feelisch et al. suggested that NO2- can be delivered to the systemic circulation and exert coronary vasodilator and cardioprotective as well as antihypertensive effects.135 NO-containing gas is effective in tissue disinfection and regulating inflammatory processes associated with acute and chronic wounds.138–140 It has been proposed that UVA-induced NO• may also have antimicrobial effects, be involved in cutaneous wound healing as well as have antitumor activity.130,141
UVA-exposure of human skin releases NO• into the circulation. In the bloodstream, NO• can reach the nervous system.129 In this way, UVA can influence transmission of nerve signals indirectly.38
However, NO• can represent, not only beneficial effects, but also toxicity, and, due to this, it is known as a Janus molecule.130 Many of the local and systemic UV-induced responses, including erythema and edema formation, inflammation, premature aging and immune suppression, can be influenced by UVA-produced NO•. Its role in the induction and in the progression of skin cancer remains uncertain. The direct toxicity of NO• is modest, but is greatly enhanced by reactions with superoxide (O2•-) to form the powerful oxidant peroxynitrite (ONOO-), which can promote oxidative damage to blood vessels and skin. Under normal conditions O2•- is rapidly removed by superoxide dismutases (SOD). NO• is quickly removed by its rapid diffusion through tissues into red blood cells where it is converted to nitrate and nitrite by a reaction with oxyhemoglobin. This limits the biological half-life of NO• in vivo to less than a second.