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Peripheral involvement of the nitric oxide-cGMP pathway in the indomethacin-induced antinociception in rat
dc.creator | Ventura-Martínez, Rosa | |
dc.creator | Déciga-Campos, Myrna | |
dc.creator | Díaz-Reval, Ma. Irene | |
dc.creator | González-Trujano, Ma. Eva | |
dc.creator | López-Muñoz, Francisco J. | |
dc.date.accessioned | 2017-06-30T03:42:19Z | |
dc.date.available | 2017-06-30T03:42:19Z | |
dc.date.issued | 2004 | es_ES |
dc.identifier | 2137 | es_ES |
dc.identifier.issn | 0014-2999 | es_ES |
dc.identifier.uri | http://repositorio.inprf.gob.mx/handle/123456789/6793 | |
dc.identifier.uri | https://doi.org/10.1016/j.ejphar.2004.09.018 | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Elsevier B.V. | es_ES |
dc.relation | 503 (1-3) 43-48 p. | es_ES |
dc.relation | versión del editor | es_ES |
dc.rights | acceso cerrado | es_ES |
dc.title | Peripheral involvement of the nitric oxide-cGMP pathway in the indomethacin-induced antinociception in rat | es_ES |
dc.type | article | es_ES |
dc.contributor.affiliation | Facultad de Medicina, Departamento de Farmacología, Universidad Nacional Autónoma de México, Ciudad Universitaria Coyoacán, C.P. 04510, México, D.F., México | es_ES |
dc.contributor.email | flopezm@prodigy.net.mx | es_ES |
dc.relation.jnabreviado | EUR J PHARMACOL | es_ES |
dc.relation.journal | European journal of pharmacology | es_ES |
dc.identifier.place | Holanda | es_ES |
dc.date.published | 2004 | es_ES |
dc.identifier.organizacion | Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz | es_ES |
dc.identifier.eissn | 1879-0712 | es_ES |
dc.identifier.doi | 10.1016/j.ejphar.2004.09.018 | es_ES |
dc.description.month | Oct | es_ES |
dc.description.abstractotrodioma | The role of nitric oxide (NO) in the antinociceptive effect of indomethacin was assessed in the pain-induced functional impairment model in the rat (PIFIR model), a model of inflammatory and chronic pain similar to that observed in clinical gout. Oral administration of indomethacin (5.6 mg/kg), a nonselective cyclooxygenase inhibitor, significantly decreased the nociceptive response elicited by uric acid injected into the knee joint of the right hind limb (2.0+/-3.0 and 149.7+/-18.0 area units [au], in the absence and the presence of indomethacin, respectively). This effect of indomethacin was reduced in nearly 50% by local pretreatment with the nonselective inhibitor of NO synthase, N G-L-nitro-arginine methyl ester (L-NAME) (72.9+/-10.7 vs. 149.7+/-18.0 au, P<0.05). On the other hand, local administration of L-arginine (a NO synthase substrate) or sodium nitroprusside (a non-enzymatic NO donor) each increased in almost 40% the antinociceptive effect of indomethacin (230.9+/-12.6 and 226.6+/-9.7 vs. 149.7+/-18.0 au, P<0.05), whereas D-arginine (the inactive isomer of arginine) had no effect on the indomethacin antinociceptive response (208.0+/-34.9 vs. 149.7+/-18.0 au). These results suggest that, the antinociceptive effect of indomethacin involves, at least in part, the NO-cyclic GMP pathway at peripheral level. | es_ES |
dc.subject.meshm | Animals | es_ES |
dc.subject.meshm | Anti-Inflammatory Agents, Non-Steroidal-Pharmacology | es_ES |
dc.subject.meshm | Arginine-Metabolism | es_ES |
dc.subject.meshm | Chronic Disease | es_ES |
dc.subject.meshm | Cyclic GMP-Physiology | es_ES |
dc.subject.meshm | Disease Models, Animal | es_ES |
dc.subject.meshm | Enzyme Inhibitors-Pharmacology | es_ES |
dc.subject.meshm | Female | es_ES |
dc.subject.meshm | Gout-Chemically induced | es_ES |
dc.subject.meshm | Gout-Complications | es_ES |
dc.subject.meshm | Gout-Psychology | es_ES |
dc.subject.meshm | Indomethacin-Pharmacology | es_ES |
dc.subject.meshm | NG-Nitroarginine Methyl | es_ES |
dc.subject.meshm | Ester-Pharmacology | es_ES |
dc.subject.meshm | Nerve Tissue Proteins-Antagonists & inhibitors | es_ES |
dc.subject.meshm | Nitric Oxide-Physiology | es_ES |
dc.subject.meshm | Nitric Oxide Donors-Pharmacology | es_ES |
dc.subject.meshm | Nitric Oxide Synthase-Antagonists & inhibitors | es_ES |
dc.subject.meshm | Nitric Oxide Synthase Type I | es_ES |
dc.subject.meshm | Nitroprusside-Pharmacology | es_ES |
dc.subject.meshm | Pain-Chemically induced | es_ES |
dc.subject.meshm | Pain-Drug therapy | es_ES |
dc.subject.meshm | Pain Measurement-Drug effects | es_ES |
dc.subject.meshm | Peripheral Nervous | es_ES |
dc.subject.meshm | System-Drug effects | es_ES |
dc.subject.meshm | Rats | es_ES |
dc.subject.meshm | Rats, Wistar | es_ES |
dc.subject.meshm | Signal Transduction-Physiology | es_ES |
dc.subject.meshm | Uric Acid | es_ES |
dc.subject.kw | Modelo PIFIR | es_ES |
dc.subject.kw | Indometacina | es_ES |
dc.subject.kw | Antinocicepción | es_ES |
dc.subject.kw | Óxido nítrico | es_ES |
dc.subject.kw | Rata | es_ES |
dc.subject.ko | PIFIR model | es_ES |
dc.subject.ko | Indomethacin | es_ES |
dc.subject.ko | Antinociception | es_ES |
dc.subject.ko | Nitric oxide | es_ES |
dc.subject.ko | Rat | es_ES |
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