Adrenergic modulation of dexketoprofen antinociception in murine formalin orofacial pain

Non-steroidal anti-inflammatory drugs (NSAIDs) are widely used in pain whose mechanism of action is the inhibition cyclooxygenase enzymes (COXs), however, there evidence other mechanisms action, such as substance P, interaction with systems NO, monoaminergic and others. The objective present work was to study participation a-1 (prazosin) a-2 (yohimbine) adrenoceptors antagonists antinociception dexketoprofen, S (+) enantiomer ketoprofen. evaluation thru mice orofacial formalin assay. Dexketoprofen (DEX) induced a dose-related 3.40 times more potent phase I than II. Prazosin i.p. decreased DEX, 2.01 4.02 Administered i.t. reduced 5.30 6.20 Yohimbine reduction ED50 4.50 II, after administration by DEX mediated activation α-1 α-2 adrenergic receptors at supraspinal spinal levels.