Nitric Oxide is produced in the skin by the sun (UVA thru IR)
Claude AI - May 2026
Question: I know that vitamin D is produced in the skin when exposed to the UVB in the summer sun from about 11AM to 2PM. I have heard that Nitric Oxide is produced by the summer sun. I suspect that for a longer portion of the day, and the hotter the day (more IR), the more is produced.
Your intuition is largely correct, and the picture is actually richer than you've laid out. The story of sunlight-induced NO has expanded considerably beyond UVA in the last decade.
| Time of day | UVB (vitamin D) | UVA + visible + NIR (NO) |
|---|---|---|
| Early morning | Negligible | Active (UVA, red, NIR) |
| 11 AM – 2 PM | Peak | Peak across all bands |
| Late afternoon | Falls off sharply | Still active |
| Cloudy/cool day | Heavily reduced | UVA partial; NIR/heat reduced |
| Hot clear day | Strong | Maximal (UVA + IR + heat-driven NOS) |
The mechanism is photolysis, not synthesis (mostly)
Sunlight doesn't make NO the way it makes vitamin D. The skin holds a substantial reservoir of photolabile nitric oxide derivatives (NODs) — primarily nitrite, nitrate, and S-nitrosothiols — and certain wavelengths cleave these to liberate free NO non-enzymatically, which then enters the systemic circulation and drops blood pressure. This non-enzymatic (without NOS involvement) photolytic reaction mobilizes cutaneous stores of NO derivatives to the bloodstream, lowering blood pressure. This is the Oplander/Liu/Weller paradigm and is now well established.
Wavelength: it's mostly UVA, not UVB
This is the key correction to your premise. UVB makes vitamin D; UVA (and longer wavelengths) releases NO. The whole of the ultraviolet A (UV-A) spectrum appears to be responsible for NO release, with efficiency higher at exposures closer to shorter UV-A wavelengths and decreasing with wavelength increases. Peak action is around 340–360 nm. Nitrite ions undergo photolysis, showing a maximum around 354 nm, and S-nitrosothiols have an absorption band peaking in the range of 330–340 nm.
This matters for your "longer portion of the day" hypothesis — and it strongly supports it. UVB requires a solar zenith angle steep enough (roughly >45°) to punch through the atmospheric ozone, which is why vitamin D production collapses outside the ~10 AM–2 PM summer window at our latitude. UVA is filtered much less by the atmosphere and is available essentially from a couple of hours after sunrise to a couple of hours before sunset. So you can reasonably expect NO-releasing wavelengths for roughly 8–12 hours on a clear summer day versus 3–4 hours for meaningful vitamin D synthesis.
Beyond UVA: blue, red, and near-infrared also release NO
This is the part that has expanded the picture dramatically. Nitric oxide can be stored in a pool of compounds readily converted to NO following skin irradiation by UVR and blue light. However, with the likelihood of skin deleterious effects caused by UVR/blue light, safer wavelengths in the red/near-infrared (NIR) spectrum are becoming potential contenders to release cutaneous NO, possibly via NOS temperature-dependent effects.
Blue light at 412–453 nm also photolytically releases NO from nitrosated proteins. And — directly relevant to your IR hypothesis — near-infrared at 850 nm released twice as much NO as visible red light at 660 nm, with the superiority of NIR possibly explained by intradermal inside-out heating via NIR water absorption.
Your IR/heat hypothesis: supported, via two mechanisms
There are at least two pathways by which a hotter day would increase NO output:
Enzymatic NOS activation by heat. Kellogg et al. described temperature-dependent enzymatic nitric oxide release from the skin, mediated by NOS, with local warming from 34 °C to 41.5 °C. This is independent of any photolytic mechanism — skin warming alone upregulates eNOS activity.
NIR-driven inside-out heating + direct photolysis. NIR can raise the temperature of the deeper skin layers without significantly affecting the surface temperature. The water in the dermis absorbs NIR photons, warming deeper tissue and likely triggering NOS-mediated NO release on top of any direct photolytic release.
(Bonus) Sweating itself releases NO. NO is physiologically released during sweating to assist in the regulation of blood flow to the skin, which aids in heat dissipation.
One caveat worth keeping in mind
NO release isn't strictly proportional to dose. UK sunlight exposure upregulates the cardio-protectant nitric oxide within in vitro skin cell lines with negligible increases in DNA damage and cell death at 1 SED. Modest, sub-erythemal exposures look most favorable on the risk/benefit ratio. There's also striking persistence: release of nitric oxide in the skin cells induced by a moderate exposure to UV-A in sunlight may be especially beneficial for some demographic groups such as the elderly, hypertensive patients or those with impaired nitric oxide function, not only during exposure but many hours and days after that.
The Barolet 2021 review (Nitric Oxide, vol. 117, pp. 16–25) and the Holliman 2017 Scientific Reports multi-cell/multi-donor analysis would be the strongest single-citation anchors for such a page. Want me to pull either of those into a citation-graded draft?