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Lesions of the commissural nucleus of the solitary tract reduce arterial pressure in spontaneously hypertensive rats

dc.contributor.authorSato, M. A.
dc.contributor.authorMenani, José Vanderlei [UNESP]
dc.contributor.authorLopes, O. U.
dc.contributor.authorColombari, Eduardo [UNESP]
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-20T13:45:43Z
dc.date.available2014-05-20T13:45:43Z
dc.date.issued2001-09-01
dc.description.abstractIt has been suggested that increased sympathetic activity and arterial chemoreceptors are important for the high blood pressure in spontaneously hypertensive rats (SHR). Electrolytic lesions of the commissural nucleus of the solitary tract (commNTS) abolish (1) the cardiovascular responses to chemoreflex activation with potassium cyanide (KCN) in normotensive rats and (2) the hypertension that follows acute aortic baroreceptor denervation in rats. Therefore, in this study we investigated the effects of electrolytic lesions of the commNTS on basal mean arterial pressure (MAP), baroreflex, and chemoreflex in SHR and in normotensive control Wistar-Kyoto (WKY) and Wistar rats. CommNTS lesions elicited a dramatic fall in MAP to normal levels during the period of Study (from the first to fourth day following lesions) in SHR and almost no changes in WKY and Wistar rats. The pressor responses to chemoreflex activation with KCN tested in the days 1 and 4 after commNTS lesions were abolished in SHR and in normotensive strains. The reflex tachycardia induced by sodium nitroprusside was also attenuated in days 1 and 4 after commNTS lesions in SHR, WKY, and Wistar rats. The data suggest that the integrity of commNTS is important for the maintenance or high blood pressure in SHR and for the reflex responses dependent on sympathetic activation either in SHR or in normotensive strains.en
dc.description.affiliationUniv Fed São Paulo, Escola Paulista Med, Dept Physiol, BR-04023060 São Paulo, Brazil
dc.description.affiliationUNESP, Fac Odontol, Dept Physiol & Pathol, Araraquara, Brazil
dc.description.affiliationUnespUNESP, Fac Odontol, Dept Physiol & Pathol, Araraquara, Brazil
dc.format.extent560-564
dc.identifierhttp://dx.doi.org/10.1161/​01.HYP.38.3.560
dc.identifier.citationHypertension. Philadelphia: Lippincott Williams & Wilkins, v. 38, n. 3, p. 560-564, 2001.
dc.identifier.doi10.1161/​01.HYP.38.3.560
dc.identifier.issn0194-911X
dc.identifier.lattes1023597870118105
dc.identifier.lattes4544450092427426
dc.identifier.urihttp://hdl.handle.net/11449/16109
dc.identifier.wosWOS:000171308400006
dc.language.isoeng
dc.publisherLippincott Williams & Wilkins
dc.relation.ispartofHypertension
dc.relation.ispartofjcr6.823
dc.rights.accessRightsAcesso restritopt
dc.sourceWeb of Science
dc.subjectbaroreceptorspt
dc.subjectchemoreceptorspt
dc.subjectsolitary nucleuspt
dc.subjectrats, spontaneously hypertensivept
dc.titleLesions of the commissural nucleus of the solitary tract reduce arterial pressure in spontaneously hypertensive ratsen
dc.typeArtigopt
dcterms.licensehttp://atvb.ahajournals.org/site/misc/ifora.xhtml#embargo
dcterms.rightsHolderLippincott Williams & Wilkins
dspace.entity.typePublication
relation.isDepartmentOfPublicationb3ba3d9c-022e-4521-8805-0bcceea7372e
relation.isDepartmentOfPublication.latestForDiscoveryb3ba3d9c-022e-4521-8805-0bcceea7372e
relation.isOrgUnitOfPublicationca4c0298-cd82-48ee-a9c8-c97704bac2b0
relation.isOrgUnitOfPublication.latestForDiscoveryca4c0298-cd82-48ee-a9c8-c97704bac2b0
unesp.author.lattes1023597870118105
unesp.author.lattes4544450092427426[4]
unesp.author.orcid0000-0002-1395-4036[4]
unesp.author.orcid0000-0003-1167-4441[2]
unesp.campusUniversidade Estadual Paulista (UNESP), Faculdade de Odontologia, Araraquarapt
unesp.departmentFisiologia e Patologia - FOARpt

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