Heat and photolytic nitric oxide are essential factors for light-induced vascular tension changes

Light induces various vascular tension changes, but these phenomena and their mechanisms remain controversial. We hypothesise that photocontraction results from the thermal effect, and that photorelaxation results from the non-thermal effect of photochemical nitric oxide generation. The isometric tension of a rat aortic ring was measured during laser light irradiation at various wavelengths with constant heat generation. Visible irradiation (458 nm, 514.5 nm) induced either photorelaxation (the tension increment was -20% of the contracted state induced by noradrenaline) or photocontraction (+7.8%); UV irradiation (351 nm) induced only photorelaxation (-41%), and near-IR irradiation (800 nm) produced only photocontraction (+11%). In the vascular tissue, photocontraction increased with deposited light energy, which was proportional to the temperature elevation. Simply heating the vascular tissue also resulted in vasocontraction. Photorelaxation by UV occurred even in the absence of endothelium, and was significantly reduced to 49% of control levels of photorelaxation by the guanylate cyclase inhibitor, methylene blue. Photorelaxation was not reduced by the nitric oxide synthetase inhibitors, ND-monomethyl-L-arginine (L-NMMA) and N(ω)-nitro-L-arginine methyl ester (L-NAME). We conclude that photocontraction is produced by the thermal effect resulting from deposited light energy. Photorelaxation might be induced by endothelium-independent nitric oxide generation, which seems to result from the photochemical effect due to photon energy.