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dc.contributor.authorDe Luca, L. A.
dc.contributor.authorSugawara, A. M.
dc.contributor.authorMenani, José Vanderlei [UNESP]
dc.date.accessioned2014-05-20T15:29:33Z
dc.date.available2014-05-20T15:29:33Z
dc.date.issued2000-05-01
dc.identifierhttp://dx.doi.org/10.1046/j.1440-1681.2000.03262.x
dc.identifier.citationClinical and Experimental Pharmacology and Physiology. Carlton: Blackwell Science Asia, v. 27, n. 5-6, p. 437-442, 2000.
dc.identifier.issn0305-1870
dc.identifier.urihttp://hdl.handle.net/11449/39121
dc.description.abstract1. Angiotensin (Ang)II is involved in responses to hypovolaemia, such as sodium appetite and increase in blood pressure, Target areas subserving these responses for AngII include the cardiovascular system in the periphery and the circumventricular organs in the brain.2. Conflicting data have been reported for the role of systemic versus brain AngII in the mediation of sodium appetite.3. The role for systemic AngII and systemic AngII receptors in the control of blood pressure in hypovolaemia is well established. In contrast with systemic injections, i.c.v injections of AngII non-peptide AT(1) and AT(2) receptor antagonists, such as losartan and PD123319, do not reduce arterial pressure in sodium-depleted (furosemide injection plus removal of ambient sodium for 24 h) rats. Thus, brain AngII receptors are likely not important for cardiovascular responses to hypovolaemia induced by sodium depletion.4. Intracerebroventricular injections of losartan or PD 123319 increase arterial pressure when injected at relatively high doses. This hypertensive effect is unlikely to be an agonist effect on brain AngII receptors, Increases in arterial pressure produced by i.c.v, losartan are attenuated by lesions of the tissue surrounding the anterior third ventricle (AV3V). The hypertensive effect of i.c.v, AngII is abolished by lesions of the AV3V.5. Hypertension induced by AngII receptor antagonists is consistent with hypotension induced by AngII acting in the brain, However, the full physiological significance of this hypotensive effect mediated by brain AngII receptors remains to be determined.en
dc.format.extent437-442
dc.language.isoeng
dc.publisherBlackwell Science Asia
dc.relation.ispartofClinical and Experimental Pharmacology and Physiology
dc.sourceWeb of Science
dc.subjectAT(1) and AT(2) receptorspt
dc.subjectblood pressurept
dc.subjectcircumventricular organspt
dc.subjectlosartanpt
dc.subjectPD123319pt
dc.subjectsodium appetitept
dc.titleBrain versus peripheral angiotensin II receptors in hypovolaemia: Behavioural and cardiovascular implicationsen
dc.typeArtigo
dcterms.licensehttp://olabout.wiley.com/WileyCDA/Section/id-406071.html
dcterms.rightsHolderBlackwell Science Asia
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.description.affiliationPaulista State Univ, UNESP, Sch Dent, Dept Physiol Sci, São Paulo, Brazil
dc.description.affiliationUnespPaulista State Univ, UNESP, Sch Dent, Dept Physiol Sci, São Paulo, Brazil
dc.identifier.doi10.1046/j.1440-1681.2000.03262.x
dc.identifier.wosWOS:000087319500021
dc.rights.accessRightsAcesso restrito
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Odontologia, Araraquarapt
dc.identifier.lattes1023597870118105
unesp.author.lattes1023597870118105
unesp.author.orcid0000-0001-8270-2652[1]
unesp.author.orcid0000-0003-1167-4441[3]
dc.relation.ispartofsjr0,759
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