Abstract.
Objective
Previous studies have found that sildenafil produces antinociception in experimental models. This work was undertaken to determine the participation of the NO/cGMP/KATP pathway in the antinociception induced by sildenafil.
Methods and results
The antinociceptive effect of sildenafil was determined in the zymosan-induced writhing response in mice. Sildenafil (1–30 mg/kg; i. p.), given 30 min before zymosan (1 mg/animal; i. p.), inhibited the writhing response (5.0 ± 1.3 versus 26.6 ± 2.7; p < 0.001) in a dose-dependent manner. L-NAME (30 mg/kg; s. c.) significantly (p < 0.05) reversed this effect (16.6 ± 3.1 versus 6.4 ± 1.6) and L-arginine (200 mg/kg; i. p.) prevented the L-NAME effect (6.8 ± 0.8 versus 16.6 ± 3.1; p < 0.05). ODQ (0,3–1 mg/kg; i. p.) and glybenclamide (0.3–1 mg/kg; p. o.) pre-treatment significantly (p < 0.01) inhibited the antinociceptive effect of sildenafil (18.0 ± 1.7 versus 2.1 ± 1.0 and 5.5 ± 0.7 versus 1.6+0.7, respectively). Diazoxide (10 mg/kg; s. c) significantly (p < 0.001) abolished the glybenclamide effect (1.6 ± 0.8 versus 14 ± 1.2).
Conclusions
The data indicate that the antinociceptive effect of sildenafil is dependent on the activation of the NO/cGMP/ KATP pathway.
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Received 10 May 2006; returned for revision 14 June 2006; accepted by G. Geisslinger 12 September 2006
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Vale, M.L., Rolim, D.E., Cavalcante, I.F. et al. Role of NO/cGMP/KATP pathway in antinociceptive effect of sildenafil in zymosan writhing response in mice. Inflamm. res. 56, 83–88 (2007). https://doi.org/10.1007/s00011-006-6109-8
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DOI: https://doi.org/10.1007/s00011-006-6109-8