Journal
EUROPEAN JOURNAL OF PHARMACOLOGY
Volume 426, Issue 1-2, Pages 39-44Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/S0014-2999(01)01206-7
Keywords
ketorolac; nitric oxide (NO); cGMP; N-G-L-nitro-arginine methyl ester (L-NAME); 1H-(1,2,4)-oxadiazolo(4,2-a)quinoxalin-1-one (ODQ); S-nitroso-N-acetylpenicillamine (SNAP); glibenclamide
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The involvement of nitric oxide (NO), cyclic GMP and ATP-sensitive K+ channels in the antinociceptive effect of ketorolac was assessed using the formalin test in the rat. Local administration of ketorolac in a formalin-injured paw produced a dose-dependent antinociceptive effect due to a local action, as drug administration in the contralateral paw was ineffective. Pretreatment of the injured paw with N-G-L-nitro-arginine methyl ester (L-NAME, an NO synthesis inhibitor), 1H-(1,2,4)-oxadiazolo(4,2-a)quinoxalin-1-one (ODQ, a soluble guanylyl cyclase inhibitor) or glibenclamide (an ATP-sensitive K+ channel blocker) prevented ketorolac-induced antinociception. However, pretreatment with saline or N-G-D-nitro-arginine methyl ester (D-NAME) did not block antinociception. Local administration of S-nitroso-N-acetylpenicillamine (SNAP, an NO donor) was inactive by itself, but increased the effect of ketorolac. The present results suggest that the antinociceptive effect of ketorolac involves activation of the NO-cyclic GMP pathway, followed by an opening of ATP-sensitive K+ channels at the peripheral level. (C) 2001 Published by Elsevier Science B.V.
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