Enhanced pressor response to carotid occlusion in commNTS-lesioned rats: possible efferent mechanisms

Página do item simplificado
dc.contributor.authorSato, Monica Akemi [UNIFESP]
dc.contributor.authorMenani, Jose Vanderlei
dc.contributor.authorLopes, Oswaldo Ubriaco [UNIFESP]
dc.contributor.authorColombari, Eduardo [UNIFESP]
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionUniv Estadual Paulista
dc.date.accessioned2018-06-15T13:20:13Z
dc.date.available2018-06-15T13:20:13Z
dc.date.issued2000-05-01
dc.description.abstractBilateral common carotid occlusion (BCO) over a period of 60 s in conscious rats produces a biphasic presser response, consisting of an early (peak) and late (plateau) phase. In this study we investigated 1) the effects of lesions of the commissural nucleus of the solitary tract (commNTS) on the cardiovascular responses produced by BCO in conscious rats and 2) the autonomic and humoral mechanisms activated to produce the presser response to BCO in sham- and commNTS-lesioned rats. Both the peak and plateau of the presser response produced by BCO increased in commNTS-lesioned rats despite the impairment of chemoreflex responses induced by intravenous potassium cyanide. In sham rats sympathetic blockade with intravenous prazosin and metoprolol, but not vasopressin receptor blockade with the Manning compound, reduced both components of BCO. In commNTS-lesioned rats the sympathetic blockade or vasopressin receptor blockade reduced both components of BCO. The results showed 1) the sympathetic nervous system, but not vasopressin, is important for the presser response to BCO during 60 s in conscious sham rats; 2) in commNTS-lesioned rats, despite chemoreflex impairment, BCO produces an increased presser response dependent on sympathetic activity associated with vasopressin release; and 3) the increment in the presser response to BCO in commNTS-lesioned rats seems to depend only on vasopressin secretion.en
dc.description.affiliationUNIFESP, Escola Paulista Med, Dept Physiol, BR-04023060 Sao Paulo, Brazil
dc.description.affiliationUniv Estadual Paulista, Fac Odontol, BR-14801903 Araraquara, SP, Brazil
dc.description.affiliationUnifespUNIFESP, Escola Paulista Med, Dept Physiol, BR-04023060 Sao Paulo, Brazil
dc.description.sourceWeb of Science
dc.format.extentR1258-R1266
dc.identifierhttp://ajpregu.physiology.org/content/278/5/R1258
dc.identifier.citationAmerican Journal Of Physiology-regulatory Integrative And Comparative Physiology. Bethesda: Amer Physiological Soc, v. 278, n. 5, p. R1258-R1266, 2000.
dc.identifier.issn0363-6119
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/42352
dc.identifier.wosWOS:000087001100020
dc.language.isoeng
dc.publisherAmer Physiological Soc
dc.relation.ispartofAmerican Journal Of Physiology-regulatory Integrative And Comparative Physiology
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectarterial pressureen
dc.subjectnucleus of the solitary tracten
dc.subjectbaroreceptoren
dc.subjectchemoreceptoren
dc.subjectpotassium cyanideen
dc.subjectsympatheticen
dc.subjectvasopressinen
dc.titleEnhanced pressor response to carotid occlusion in commNTS-lesioned rats: possible efferent mechanismsen
dc.typeinfo:eu-repo/semantics/article
Arquivos
Coleções
EPM - Artigos