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dc.contributor.authorSato, M. A.-
dc.contributor.authorMenani, José Vanderlei-
dc.contributor.authorLopes, O. U.-
dc.contributor.authorColombari, Eduardo-
dc.identifier.citationAmerican Journal of Physiology-regulatory Integrative and Comparative Physiology. Bethesda: Amer Physiological Soc, v. 278, n. 5, p. R1258-R1266, 2000.-
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.publisherAmer Physiological Soc-
dc.sourceWeb of Science-
dc.subjectarterial pressurept
dc.subjectnucleus of the solitary tractpt
dc.subjectpotassium cyanidept
dc.titleEnhanced pressor response to carotid occlusion in commNTS-lesioned rats: possible efferent mechanismsen
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)-
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)-
dc.description.affiliationUNIFESP, Escola Paulista Med, Dept Physiol, BR-04023060 São Paulo, Brazil-
dc.description.affiliationUniv Estadual Paulista, Fac Odontol, BR-14801903 Araraquara, SP, Brazil-
dc.description.affiliationUnespUniv Estadual Paulista, Fac Odontol, BR-14801903 Araraquara, SP, Brazil-
dc.rights.accessRightsAcesso aberto-
dc.relation.ispartofAmerican Journal of Physiology: Regulatory Integrative and Comparative Physiology-
Appears in Collections:Artigos, TCCs, Teses e Dissertações da Unesp

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