This work evaluated the analgesic and anti-inflammatory activity of the ruthenium(II) complexes trans-[Ru(NO+)(NH3)4(L)](BF4)3 and [Ru(NH3)5(L)](BF4)3 containing the nonsteroidal anti-inflammatory drugs nicotinic acid (Hnic) and its isomer isonicotinic acid (ina) as ligands (L). The antinociceptive potential of these complexes and the free ligands (non-coordinated to ruthenium) was tested in different models with doses ranging from 1 to 100 µmol/kg. The ligands themselves were inactive; however, the ruthenium complexes containing Hnic and ina inhibited mechanical hyperalgesia induced by prostaglandin E2, carrageenan-induced hyperalgesia and antigen-induced arthritis. Moreover, the ruthenium complexes inhibited overt nociception induced by formalin, acetic acid, capsaicin and cinnamaldehyde. The mechanism involved in the antinociceptive effects of the ruthenium complexes suggested that ATP-sensitive K+ channel pathways were not involved because glibenclamide did not affect their antinociceptive activities. However, the antinociceptive effect appears to be a consequence of the reduction in neutrophil migration and inhibition of the protein kinase C pathway.