Role Of The No-Cgmp-K+ Channels Pathway In The Peripheral Antinociception Induced By Alpha-Bisabolol

The aim of this study was to examine if the peripheral antinociception of alpha-bisabolol involves the participation of nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) synthesis followed by K+ channel opening in the formalin test. Wistar rats were injected in the dorsal surface of the right hind paw with formalin (1%). Rats received a subcutaneous injection into the dorsal surface of the paw of vehicles or increasing doses of alpha-bisabolol (100-300 mu g/paw). To determine whether the peripheral antinociception induced by alpha-bisabolol was mediated by either the opioid receptors or the NOcGMP-r channels pathway, the effect of pretreatment (10 min before formalin injection) with the appropriate vehicles, naloxone, naltrexone, N-G-nitro-t-arginine methyl ester (L-NAME), 1R[1,2,4]-oxadiazolo[4,2-alquinoxalin-1-one (ODQ), glibenclamide, glipizide, apamin, charybdotoxin, tetraethylammonium, or 4-aminopyridine on the antinociceptive effects induced by local peripheral alpha-bisabolol (300 mu g/paw) were assessed. a-Bisabolol produced antinociception during both phases of the formalin test. ot-Bisabolol antinociception was blocked by L-NAME, ODQ, and all the K+ channels blockers. The peripheral antinociceptive effect produced by alpha-bisabolol was not blocked by the opioid receptor inhibitors. alpha-Bisabolol was able to active the NO-cGMP-K+ channels pathway to produce its antinoceptive effect. The participation of opioid receptors in the peripheral local antinociception induced by alpha-bisabolol is excluded.