INVOLVEMENT OF NITRIC-OXIDE SYNTHASE IN THE DELAYED VASODILATOR RESPONSE TO ULTRAVIOLET-LIGHT IRRADIATION OF RAT SKIN IN-VIVO

1 The role of nitric oxide synthase and cyclo-oxygenase in the skin blood flow response to ultraviolet light B (u.v.B) irradiation was investigated in the rat in vivo. 2 Local skin blood flow changes were measured in the shaved dorsal skin of anaesthetized male Sprague-Dawley rats with a laser Doppler flow probe. 3 u.v.B irradiation caused delayed onset vasodilatation and by 18 h basal blood flow increased by 125 +/- 25% (P<0.05, n = 12 rats, mean +/- s.e.mean). 4 Indomethacin, 3 nmol per site, N(G)-nitro-L-arginine methyl ester (L-NAME) 100 nmol per site, but not D-NAME 100 nmol per site, injected locally 17.5 h after u.v.B irradiation abolished the 18 h increase in blood flow. 5 The nitric oxide synthase inhibitor L-NAME, N(G)-monomethyl-L-arginine (L-NMMA) and canavanine, 10 and 100 nmol per site injected at 17.5 h, suppressed significantly the u.v.B 18 h response in a dose-dependent manner. The order of potency was L-NAME > canavanine = L-NMMA. The effect of L-NAME was reversed partially by the co-injection of an exceSS Of L-arginine. 6 Topical application of the corticosteroid, clobetasol 17-propionate, immediately after irradiation inhibited the 18 h u.v.B response in a dose-dependent manner. 7 The delayed onset microcirculatory vasodilatation induced by u.v.B involves both nitric oxide synthase and cyclo-oxygenase in this in vivo model. Topical corticosteroids may attenuate the response by inhibiting both prostaglandin and nitric oxide synthesis pathways.