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Ang-(1-7) activates the NO/cGMP and ATP-sensitive K+ channels pathway to induce peripheral antinociception in rats.
Costa, Aline; Galdino, Giovane; Romero, Thiago; Silva, Grazielle; Cortes, Steyner; Santos, Robson; Duarte, Igor.
Afiliação
  • Costa A; Department of Pharmacology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil.
  • Galdino G; Department of Pharmacology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil.
  • Romero T; Department of Pharmacology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil.
  • Silva G; Department of Pharmacology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil.
  • Cortes S; Department of Pharmacology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil.
  • Santos R; Department of Physiology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil.
  • Duarte I; Department of Pharmacology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil. Electronic address: dimitri@icb.ufmg.br.
Nitric Oxide ; 37: 11-6, 2014 Feb 15.
Article em En | MEDLINE | ID: mdl-24361899
Angiotensin-(1-7) is a bioactive component of the renin-angiotensin system that is formed endogenously and induces nitric oxide release in several tissues. The L-arginine/NO/cyclic GMP pathway and ATP-sensitive K+ channels have been proposed as the mechanism of action for the peripheral antinociception of several groups of drug and endogenous substances, including opioids, non-steroidal analgesics, acetylcholine and others. The aim of the present study was to investigate the involvement of the L-arginine/NO/cGMP and KATP+ pathway on antinociception induced by angiotensin-(1-7). Paw pressure in rats was used to induce hyperalgesia via an intraplantar injection of prostaglandin E2 (2 µg/paw). Ang-(1-7) (2, 3 and 4 µg/paw) elicited a local peripheral antinociceptive effect that was antagonized by the nonselective NO synthase (NOS) inhibitor L-NOarg and the selective neuronal NOS (nNOS) inhibitor L-NPA. The selective inhibition of endothelial (eNOS) and inducible (iNOS) NOS by L-NIO and L-NIL, respectively, was ineffective at blocking the effects of a local Ang-(1-7) injection. In addition, the level of nitrite in the homogenized paw tissue, as determined by a colorimetric assay, indicated that exogenous Ang-(1-7) is able to induce NO release. The soluble guanylyl cyclase inhibitor ODQ and the specific blocker of ATP-sensitive K+ channels glibenclamide (40, 80 and 160 µg/paw) antagonized the Ang-(1-7) response. The results provide evidence that Ang-(1-7) most likely induces peripheral antinociceptive effects via the L-arginine/NO/cGMP pathway and KATP+ pathway activation.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Dor / Fragmentos de Peptídeos / Angiotensina I / Trifosfato de Adenosina / GMP Cíclico / Canais KATP / Analgésicos / Óxido Nítrico Tipo de estudo: Diagnostic_studies Limite: Animals Idioma: En Revista: Nitric Oxide Assunto da revista: BIOQUIMICA / QUIMICA Ano de publicação: 2014 Tipo de documento: Article País de afiliação: Brasil País de publicação: Estados Unidos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Dor / Fragmentos de Peptídeos / Angiotensina I / Trifosfato de Adenosina / GMP Cíclico / Canais KATP / Analgésicos / Óxido Nítrico Tipo de estudo: Diagnostic_studies Limite: Animals Idioma: En Revista: Nitric Oxide Assunto da revista: BIOQUIMICA / QUIMICA Ano de publicação: 2014 Tipo de documento: Article País de afiliação: Brasil País de publicação: Estados Unidos