Possible involvement of L-arginine-nitric oxide pathway in the modulation of stress-induced analgesia.

The possible participation of NO in the pain modulation and stress analgesia was studied in Wistar adult rats. Cerebral citruline as a stoichiometric coproduct of NO from L-arginine increased from the mean value 5.6 +/- 0.4 nM/mg.Pt. to 8.9 +/- 0.5 nM/mg.Pt. in acute immobilization stress. Intraperitoneal administration of L-arginine caused only in high doses (50 mg/kg body weight) a small transient decrease of tail-flick latencies to the thermoalgesic stimulus, without significant changes of the stress analgesia induced by the restraint stress. In the pretreated animals with L-NAME a progressive increase of latency time was obtained and the increased latencies induced by acute immobilization appeared significantly potentiated. These results offer new indirect evidence in favour of the modulatory role of NO in the thermoalgesic sensitivity and stress induced analgesia.