Tranilast increases vasodilator response to acetylcholine in rat mesenteric resistance arteries through increased EDHF participation

Background and Purpose: Tranilast, in addition to its capacity to inhibit mast cell degranulation, has other biological effects, including inhibition of reactive oxygen species, cytokines, leukotrienes and prostaglandin release. In the current study, we analyzed whether tranilast could alter endothe...

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Autores: Xavier, Fabiano Elias, Blanco Rivero, Javier, Sastre, Esther, Caracuel, Laura, Callejo, María, Balfagón Calvo, Gloria
Tipo de recurso: artículo
Fecha de publicación:2014
País:España
Institución:Universidad Autónoma de Madrid
Repositorio:Biblos-e Archivo. Repositorio Institucional de la UAM
Idioma:inglés
OAI Identifier:oai:repositorio.uam.es:10486/666070
Acceso en línea:http://hdl.handle.net/10486/666070
https://dx.doi.org/10.1371/journal.pone.0100356
Access Level:acceso abierto
Palabra clave:animal cell
cellular distribution
mast cell
mesenteric artery
vascular endothelium
vasodilatation
Medicina
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spelling Tranilast increases vasodilator response to acetylcholine in rat mesenteric resistance arteries through increased EDHF participationXavier, Fabiano EliasBlanco Rivero, JavierSastre, EstherCaracuel, LauraCallejo, MaríaBalfagón Calvo, Gloriaanimal cellcellular distributionmast cellmesenteric arteryvascular endotheliumvasodilatationMedicinaBackground and Purpose: Tranilast, in addition to its capacity to inhibit mast cell degranulation, has other biological effects, including inhibition of reactive oxygen species, cytokines, leukotrienes and prostaglandin release. In the current study, we analyzed whether tranilast could alter endothelial function in rat mesenteric resistance arteries (MRA). Experimental Approach: Acetylcholine-induced relaxation was analyzed in MRA (untreated and 1-hour tranilast treatment) from 6 month-old Wistar rats. To assess the possible participation of endothelial nitric oxide or prostanoids, acetylcholineinduced relaxation was analyzed in the presence of L-NAME or indomethacin. The participation of endothelium-derived hyperpolarizing factor (EDHF) in acetylcholine-induced response was analyzed by preincubation with TRAM-34 plus apamin or by precontraction with a high K+ solution. Nitric oxide (NO) and superoxide anion levels were measured, as well as vasomotor responses to NO donor DEA-NO and to large conductance calcium-activated potassium channel opener NS1619. Key Results: Acetylcholine-induced relaxation was greater in tranilast-incubated MRA. Acetylcholine-induced vasodilation was decreased by L-NAME in a similar manner in both experimental groups. Indomethacin did not modify vasodilation. Preincubation with a high K+ solution or TRAM-34 plus apamin reduced the vasodilation to ACh more markedly in tranilastincubated segments. NO and superoxide anion production, and vasodilator responses to DEA-NO or NS1619 remained unmodified in the presence of tranilast. Conclusions and Implications: Tranilast increased the endothelium-dependent relaxation to acetylcholine in rat MRA. This effect is independent of the nitric oxide and cyclooxygenase pathways but involves EDHF, and is mediated by an increased role of small conductance calcium-activated K+ channelsThis study was supported by Ministerio de Ciencia e Innovación (SAF 2009-10374), Ministerio de Economía y Competitividad (SAF 2012-38530), and Fundación Mapfre. F.E. Xavier is recipient of research fellowship from Conselho Nacional de Desenvolvimento Científico e Tecnológico (Brazil)Public Library of ScienceDepartamento de FisiologíaFacultad de Medicina20142014-07-03research articlehttp://purl.org/coar/resource_type/c_2df8fbb1VoRhttp://purl.org/coar/version/c_970fb48d4fbd8a85info:eu-repo/semantics/articleapplication/pdfhttp://hdl.handle.net/10486/666070https://dx.doi.org/10.1371/journal.pone.0100356reponame:Biblos-e Archivo. Repositorio Institucional de la UAMinstname:Universidad Autónoma de MadridInglésengopen accesshttp://purl.org/coar/access_right/c_abf2info:eu-repo/semantics/openAccessoai:repositorio.uam.es:10486/6660702026-06-23T12:46:27Z
dc.title.none.fl_str_mv Tranilast increases vasodilator response to acetylcholine in rat mesenteric resistance arteries through increased EDHF participation
title Tranilast increases vasodilator response to acetylcholine in rat mesenteric resistance arteries through increased EDHF participation
spellingShingle Tranilast increases vasodilator response to acetylcholine in rat mesenteric resistance arteries through increased EDHF participation
Xavier, Fabiano Elias
animal cell
cellular distribution
mast cell
mesenteric artery
vascular endothelium
vasodilatation
Medicina
title_short Tranilast increases vasodilator response to acetylcholine in rat mesenteric resistance arteries through increased EDHF participation
title_full Tranilast increases vasodilator response to acetylcholine in rat mesenteric resistance arteries through increased EDHF participation
title_fullStr Tranilast increases vasodilator response to acetylcholine in rat mesenteric resistance arteries through increased EDHF participation
title_full_unstemmed Tranilast increases vasodilator response to acetylcholine in rat mesenteric resistance arteries through increased EDHF participation
title_sort Tranilast increases vasodilator response to acetylcholine in rat mesenteric resistance arteries through increased EDHF participation
dc.creator.none.fl_str_mv Xavier, Fabiano Elias
Blanco Rivero, Javier
Sastre, Esther
Caracuel, Laura
Callejo, María
Balfagón Calvo, Gloria
author Xavier, Fabiano Elias
author_facet Xavier, Fabiano Elias
Blanco Rivero, Javier
Sastre, Esther
Caracuel, Laura
Callejo, María
Balfagón Calvo, Gloria
author_role author
author2 Blanco Rivero, Javier
Sastre, Esther
Caracuel, Laura
Callejo, María
Balfagón Calvo, Gloria
author2_role author
author
author
author
author
dc.contributor.none.fl_str_mv Departamento de Fisiología
Facultad de Medicina
dc.subject.none.fl_str_mv animal cell
cellular distribution
mast cell
mesenteric artery
vascular endothelium
vasodilatation
Medicina
topic animal cell
cellular distribution
mast cell
mesenteric artery
vascular endothelium
vasodilatation
Medicina
description Background and Purpose: Tranilast, in addition to its capacity to inhibit mast cell degranulation, has other biological effects, including inhibition of reactive oxygen species, cytokines, leukotrienes and prostaglandin release. In the current study, we analyzed whether tranilast could alter endothelial function in rat mesenteric resistance arteries (MRA). Experimental Approach: Acetylcholine-induced relaxation was analyzed in MRA (untreated and 1-hour tranilast treatment) from 6 month-old Wistar rats. To assess the possible participation of endothelial nitric oxide or prostanoids, acetylcholineinduced relaxation was analyzed in the presence of L-NAME or indomethacin. The participation of endothelium-derived hyperpolarizing factor (EDHF) in acetylcholine-induced response was analyzed by preincubation with TRAM-34 plus apamin or by precontraction with a high K+ solution. Nitric oxide (NO) and superoxide anion levels were measured, as well as vasomotor responses to NO donor DEA-NO and to large conductance calcium-activated potassium channel opener NS1619. Key Results: Acetylcholine-induced relaxation was greater in tranilast-incubated MRA. Acetylcholine-induced vasodilation was decreased by L-NAME in a similar manner in both experimental groups. Indomethacin did not modify vasodilation. Preincubation with a high K+ solution or TRAM-34 plus apamin reduced the vasodilation to ACh more markedly in tranilastincubated segments. NO and superoxide anion production, and vasodilator responses to DEA-NO or NS1619 remained unmodified in the presence of tranilast. Conclusions and Implications: Tranilast increased the endothelium-dependent relaxation to acetylcholine in rat MRA. This effect is independent of the nitric oxide and cyclooxygenase pathways but involves EDHF, and is mediated by an increased role of small conductance calcium-activated K+ channels
publishDate 2014
dc.date.none.fl_str_mv 2014
2014-07-03
dc.type.none.fl_str_mv research article
http://purl.org/coar/resource_type/c_2df8fbb1
VoR
http://purl.org/coar/version/c_970fb48d4fbd8a85
dc.type.openaire.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.none.fl_str_mv http://hdl.handle.net/10486/666070
https://dx.doi.org/10.1371/journal.pone.0100356
url http://hdl.handle.net/10486/666070
https://dx.doi.org/10.1371/journal.pone.0100356
dc.language.none.fl_str_mv Inglés
eng
language_invalid_str_mv Inglés
language eng
dc.rights.none.fl_str_mv open access
http://purl.org/coar/access_right/c_abf2
dc.rights.openaire.fl_str_mv info:eu-repo/semantics/openAccess
rights_invalid_str_mv open access
http://purl.org/coar/access_right/c_abf2
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Public Library of Science
publisher.none.fl_str_mv Public Library of Science
dc.source.none.fl_str_mv reponame:Biblos-e Archivo. Repositorio Institucional de la UAM
instname:Universidad Autónoma de Madrid
instname_str Universidad Autónoma de Madrid
reponame_str Biblos-e Archivo. Repositorio Institucional de la UAM
collection Biblos-e Archivo. Repositorio Institucional de la UAM
repository.name.fl_str_mv
repository.mail.fl_str_mv
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score 15,300719

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