dc.contributor.author | Sastre, Esther | |
dc.contributor.author | Caracuel, Laura | |
dc.contributor.author | Xavier, Fabiano Elias | |
dc.contributor.author | Balfagón Calvo, Gloria | |
dc.contributor.author | Blanco Rivero, Javier | |
dc.contributor.other | UAM. Departamento de Fisiología | es_ES |
dc.date.accessioned | 2015-05-12T11:41:12Z | |
dc.date.available | 2015-05-12T11:41:12Z | |
dc.date.issued | 2013-01-01 | |
dc.identifier.citation | Plos One 8.8 (2013): e73232 | en_US |
dc.identifier.issn | 1932-6203 (online) | en_US |
dc.identifier.uri | http://hdl.handle.net/10486/666136 | |
dc.description.abstract | Objectives: We analyzed whether mast cell stabilization by either ketotifen or tranilast could alter either sympathetic
or nitrergic innervation function in rat mesenteric arteries.
Methods: Electrical field stimulation (EFS)-induced contraction was analyzed in mesenteric segments from 6-monthold
Wistar rats in three experimental groups: control, 3-hour ketotifen incubated (0.1 αmol/L), and 3-hour tranilast
incubated (0.1 mmol/L). To assess the possible participation of nitrergic or sympathetic innervation, EFS contraction
was analyzed in the presence of non-selective nitric oxide synthase (NOS) inhibitor L-NAME (0.1 mmol/L), α-
adrenergic receptor antagonist phentolamine (0.1 μmol/L), or the neurotoxin 6-hydroxydopamine (6-OHDA, 1.46
mmol/L). Nitric oxide (NO) and superoxide anion (O2
.-) levels were measured, as were vasomotor responses to
noradrenaline (NA) and to NO donor DEA-NO, in the presence and absence of 0.1 mmol/L tempol. Phosphorylated
neuronal NOS (P-nNOS) expression was also analyzed.
Results: EFS-induced contraction was increased by ketotifen and decreased by tranilast. L-NAME increased the
vasoconstrictor response to EFS only in control segments. The vasodilator response to DEA-NO was higher in
ketotifen- and tranilast-incubated segments, while tempol increased vasodilator response to DEA-NO only in control
segments. Both NO and O2
- release, and P-nNOS expression were diminished by ketotifen and by tranilast
treatment. The decrease in EFS-induced contraction produced by phentolamine was lower in tranilast-incubated
segments. NA vasomotor response was decreased only by tranilast. The remnant vasoconstriction observed in
control and ketotifen-incubated segments was abolished by 6-OHDA.
Conclusion: While both ketotifen and tranilast diminish nitrergic innervation function, only tranilast diminishes
sympathetic innnervation function, thus they alter the vasoconstrictor response to EFS in opposing manners | en_US |
dc.description.sponsorship | This work was supported by grants from Ministerio de Ciencia e Innovación (SAF2009-10374), Ministerio de Economía y Competitividad
(SAF2012-38530) and Fundación Mapfre | en_US |
dc.format.extent | 10 pag. | es_ES |
dc.format.mimetype | application/pdf | en |
dc.language.iso | eng | en |
dc.publisher | Public Library of Science | en_US |
dc.relation.ispartof | Plos One | en_US |
dc.rights | © 2013 Sastre et al. | es_ES |
dc.subject.other | Acetylcholine | en_US |
dc.subject.other | Electric Stimulation | en_US |
dc.subject.other | In Vitro Techniques | en_US |
dc.subject.other | Mast Cells | en_US |
dc.subject.other | Mesenteric Arteries | en_US |
dc.subject.other | Vasoconstriction | en_US |
dc.title | Opposite effect of mast cell stabilizers ketotifen and tranilast on the vasoconstrictor response to electrical field stimulation in rat mesenteric artery | en_US |
dc.type | article | en |
dc.subject.eciencia | Medicina | es_ES |
dc.identifier.doi | 10.1371/journal.pone.0073232 | es_ES |
dc.identifier.publicationfirstpage | e73232 | es_ES |
dc.identifier.publicationissue | 8 | es_ES |
dc.identifier.publicationlastpage | e73232 | es_ES |
dc.identifier.publicationvolume | 8 | es_ES |
dc.type.version | info:eu-repo/semantics/publishedVersion | en |
dc.rights.cc | Reconocimiento | es_ES |
dc.rights.accessRights | openAccess | en |
dc.authorUAM | Sastre Gil, Esther (264491) | |
dc.facultadUAM | Facultad de Medicina | |
dc.institutoUAM | Instituto de Investigación Sanitaria Hospital Universitario de La Paz (IdiPAZ) | |