Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/43886
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dc.contributor.authorColombari, Debora Simões de Almeida [UNIFESP]
dc.contributor.authorCravo, Sergio Luiz [UNIFESP]
dc.date.accessioned2018-06-15T17:38:26Z-
dc.date.available2018-06-15T17:38:26Z-
dc.date.issued1999-10-01
dc.identifierhttps://doi.org/10.1161/01.HYP.34.4.762
dc.identifier.citationHypertension. Philadelphia: Lippincott Williams & Wilkins, v. 34, n. 4, p. 762-767, 1999.
dc.identifier.issn0194-911X
dc.identifier.urihttp://repositorio.unifesp.br/11600/43886-
dc.description.abstractThe role of the anteroventral third ventricle (AV3V) region in the cardiovascular adjustments to volume expansion (VE) with 4% Ficoll (1% body weight, 1.4 mL/min) was studied in urethane-anesthetized rats. In sham-lesioned animals, VE produced a transitory (less than or equal to 20 minutes) increase in mean arterial pressure, which peaked at 10 minutes (10+/-3 mm Hg), and sustained increases of renal (123+/-10% and 127+/-6% of baseline, respectively, 10 and 40 minutes after VE) and hindlimb vascular (157+/-19% and 153+/-9% of baseline) conductance. After AV3V lesions, VE induced a sustained increase in mean arterial pressure. Although renal blood flow increased in response to VE, renal vascular conductance was unaffected, indicating that renal vasodilation was abolished. On the other hand, after AV3V lesions, the increases in hindlimb blood flow and vascular conductance were higher than those observed in sham-lesioned rats. Results obtained demonstrated that the AV3V region is essential for the renal vasodilation induced by VE.en
dc.format.extent762-767
dc.language.isoeng
dc.publisherLippincott Williams & Wilkins
dc.relation.ispartofHypertension
dc.rightsAcesso aberto
dc.subjectblood flow velocityen
dc.subjectbrainen
dc.subjectratsen
dc.subjectblood pressureen
dc.subjectwater-electrolyte balanceen
dc.titleEffects of acute AV3V lesions on renal and hindlimb vasodilation induced by volume expansionen
dc.typeArtigo
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.description.affiliationUniv Fed Sao Paulo, Escola Paulista Med, Dept Physiol, BR-04023900 Sao Paulo, Brazil
dc.description.affiliationUnifespUniv Fed Sao Paulo, Escola Paulista Med, Dept Physiol, BR-04023900 Sao Paulo, Brazil
dc.identifier.doi10.1161/01.HYP.34.4.762
dc.description.sourceWeb of Science
dc.identifier.wosWOS:000083486500011
Appears in Collections:Artigo

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