Neurogenic oedema and vasodilatation: effect of a selective neuronal NO inhibitor

The effects of a neuronal nitric oxide synthase (nNOS) inhibitor, 1-(2-trifluoromethylphenyl)imidazole (TRIM) on rat sensory saphenous nerve-induced neurogenic inflammation were investigated. TRIM (50 mg kg-1, i.p.), but not 2-trifluoromethylphenol (TRIMPOH) which lacks nNOS inhibitory activity, inhibited neurogenic oedema by 55.8 +/- 6.5% (n = 6, p < 0.05). The effect of TRIM was partially reversed by L-arginine (100 mg kg-1, i.v., p < 0.01). TRIM also caused a reduction (p < 0.05) in neurogenic vasodilatation but had no effect on neuropeptide responses induced by substance P + CGRP. Topically applied TRIM (100 microliters of 150-250 mg ml-1) inhibited neurogenic oedema (p < 0.01). Thus, use of this recently described nNOS inhibitor has provided new evidence to further the hypothesis that nNOS plays a role in modulating sensory nerve-mediated neurogenic inflammation.