The balloon catheter induces an increase in contralateral carotid artery reactivity to angiotensin II and phenylephrine

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dc.contributor.authorAccorsi-Mendonca, D.
dc.contributor.authorCorrea, FMA
dc.contributor.authorPaiva, Therezinha B. [UNIFESP]
dc.contributor.authorSouza, H. P. de
dc.contributor.authorLaurindo, FRM
dc.contributor.authorOliveira, A. M. de
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2016-01-24T12:37:07Z
dc.date.available2016-01-24T12:37:07Z
dc.date.issued2004-05-01
dc.description.abstract1 the effects of balloon injury on the reactivity of ipsilateral and contralateral carotid arteries were compared to those observed in arteries from intact animals (control arteries).2 Carotid arteries were obtained from Wistar rats 2, 4, 7, 15, 30 or 45 days after injury and mounted in an isolated organ bath. Reactivity to angiotensin II (Ang II), phenylephrine (Phe) and bradykinin (BK) was studied. Curves were constructed in the absence or presence of endothelium or after incubation with 10 muM indomethacin, 500 muM valeryl salicylate or 0.1 muM celecoxib.3 Phe, Ang II and BK maximum effects (Emax) were decreased in ipsilateral arteries when compared to control arteries. No differences were observed among pD2 or Hill coefficient.4 Emax to Phe (4 and 7 days) and to Ang II (15 and 30 days) increased in the contralateral artery. in addition, Phe or Ang II reactivity was not significantly different in aorta rings from control or carotid-injured animals.5 the increased responsiveness of contralateral artery was not due to changes in carotid blood flow or resting membrane potential. the endothelium-dependent inhibitory component is not present in the contraction of contralateral arteries and it is not related to superoxide anion production.6 Indomethacin decreased contralateral artery responsiveness to Phe and Ang II. Valeryl salicylate reduced the Ang II response in contralateral and control arteries. Celecoxib decreased the Phe Emax of contralateral artery.7 in conclusion, decreased endothelium-derived factors and increased prostanoids appear to be responsible for the increased reactivity of contralateral arteries after injury.en
dc.description.affiliationUSP, Sch Med Ribeirao Preto, Dept Pharmacol, Ribeirao Preto, Brazil
dc.description.affiliationUNIFESP, Dept Biophys, São Paulo, Brazil
dc.description.affiliationUSP, Sch Med, Dept Emergency Med, Ribeirao Preto, Brazil
dc.description.affiliationUSP, Sch Med, Heart Inst InCor, Ribeirao Preto, Brazil
dc.description.affiliationUSP, Sch Pharm Ribeirao Preto, Pharmacol Lab, Ribeirao Preto, Brazil
dc.description.affiliationUnifespUNIFESP, Dept Biophys, São Paulo, Brazil
dc.description.sourceWeb of Science
dc.format.extent79-88
dc.identifierhttp://dx.doi.org/10.1038/sj.bjp.0705732
dc.identifier.citationBritish Journal of Pharmacology. London: Nature Publishing Group, v. 142, n. 1, p. 79-88, 2004.
dc.identifier.doi10.1038/sj.bjp.0705732
dc.identifier.issn0007-1188
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/27716
dc.identifier.wosWOS:000221589800013
dc.language.isoeng
dc.publisherNature Publishing Group
dc.relation.ispartofBritish Journal of Pharmacology
dc.rightsAcesso aberto
dc.subjectballoon catheteren
dc.subjectcontralateral arteryen
dc.subjectangiotensin IIen
dc.subjectphenylephrineen
dc.subjectcarotiden
dc.subjectvascular reactivityen
dc.titleThe balloon catheter induces an increase in contralateral carotid artery reactivity to angiotensin II and phenylephrineen
dc.typeArtigo
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