It is generally acknowledged that the cutaneous vasodilatation to monopolar galvanic current application would result from an axon reflex in primary afferent fibres and to the neurogenic inflammation resulting from neuropeptide release. Previous papers have suggested a participation of prostaglandin (PG) in anodal current-induced cutaneous vasodilatation. Thus, the inducible cyclooxygenase isoform (COX-2), assumed to play a key role in inflammation, should be involved in the synthesis of the PG released. Skin blood flow (SkBF) variations induced by 5-min, 0.1-mA monopolar anodal current application was evaluated with laser-Doppler flowmetry on the forearm of healthy volunteers under indomethacin (COX-1&2 inhibitor), celecoxib (COX-2 inhibitor) or placebo treatment. SkBF was indexed as cutaneous vascular conductance (CVC) expressed as percent of heatinduced maximal CVC (%MVC). Urinalyses were performed to test celecoxib treatment efficiency. No difference was found in CVC values at rest: 14.3 ± 4.0, 11.9 ± 3.2, 10.9 ± 2.0 %MVC after indomethacin, celecoxib or placebo treatment, respectively. At 10-min following the onset of anodal current application, CVC values were 22.2 ± 4.9 %MVC, (non-significant from rest) under indomethacin, 85.7 ± 15.3 %MVC (p<0.001 from rest) under celecoxib and 70.4 ± 13.1 %MVC (p<0.001 from rest) under placebo. Celecoxib treatment significantly depressed the urinary prostacyclin metabolite 6-keto PGF1alpha (p<0.05 from placebo). Indomethacin but not celecoxib treatment significantly inhibited the anodal current-induced vasodilatation. Thus, although assumed to result from an axon reflex in primary afferent fibres and neurogenic inflammation, these results suggest that the early anodal current-induced vasodilatation is mainly dependent on COX-1 prostaglandin synthesis.