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Please use this identifier to cite or link to this item: http://acervodigital.unesp.br/handle/11449/68736
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dc.contributor.authorSaad, Wilson Abrão-
dc.contributor.authorGuarda, I. F. M. S.-
dc.contributor.authorCamargo, L. A. D. A.-
dc.contributor.authorGuarda, R. S.-
dc.contributor.authorSantos, T. A. F. B. D.-
dc.date.accessioned2014-05-27T11:21:47Z-
dc.date.accessioned2016-10-25T18:21:51Z-
dc.date.available2014-05-27T11:21:47Z-
dc.date.available2016-10-25T18:21:51Z-
dc.date.issued2006-01-01-
dc.identifierhttp://dx.doi.org/10.3923/jbs.2006.182.186-
dc.identifier.citationJournal of Biological Sciences, v. 6, n. 1, p. 182-186, 2006.-
dc.identifier.issn1727-3048-
dc.identifier.issn1812-5719-
dc.identifier.urihttp://hdl.handle.net/11449/68736-
dc.identifier.urihttp://acervodigital.unesp.br/handle/11449/68736-
dc.description.abstractAs several structures of the central nervous system are involved in the control of hydromineral and cardiovascular balance we investigated whether the natriorhexigenic and pressor response induced by the injection of ANG II into the 3rd V could be mediated by vasopressinergic and nitrergic system. Male Holtzman rats weighing 200-250 g with cannulae implanted into the 3rd V were used. The drugs were injected in 0.5 μL over 30-60 sec. Controls were injected with a similar volume of 0.15 M NaCl. ANGII increased the water intake vs control. AVPA injected into 3rd V prior to ANGII decreased the dipsogenic effect of ANGII. L-arginine also decreased the water intake induced by ANGII. AVPA plus L-arginine inhibit the water intake induced by ANGII. 7NIT injected prior to ANGII potentiated the dipsogenic effect of ANGII. Pre-treatment with ANGII increased the sodium ingestion vs control. AVPA decreased the ANGII effect in sodium intake. L-arginine also decreased the natriorhexigenic effect of ANGII. The combination of L-arginine and AVPA inhibit the sodium intake induced by ANGII. 7NIT injected prior to ANGII potentiated the sodium intake induced by ANGII. ANGII induced an increase in Mean Arterial Pressure (MAP) vs control. AVPA and L-arginine induced a decreased in the pressor effect of ANGII. The combination of L-arginine and AVPA inhibit the pressor effect of ANGII. 7NIT injected prior to ANGII into 3rd V potentiated the pressor effect of ANGII. These data suggest that arginine vasopressin V 1 receptors and Nitric Oxide (NO) within the circumventricular structures may be involved in sodium intake and pressor response induced by the activation of ANGII receptors within the circumventricular neurons. These studies revealed the involvement of sodium appetite by utilizing the angiotensinergic, vasopressinergic and nitrergic system in the central regulation of blood pressure. © 2006 Asian Network for Scientific Information.en
dc.format.extent182-186-
dc.language.isoeng-
dc.sourceScopus-
dc.subjectANGII AVP V 1 receptors-
dc.subjectCNS-
dc.subjectNO-
dc.subjectSodium appetite an blood pressure-
dc.subject7 nitroindazole-
dc.subjectangiotensin II-
dc.subjectangiotensin receptor-
dc.subjectarginine-
dc.subjectargipressin receptor-
dc.subjectnitric oxide-
dc.subjectsodium chloride-
dc.subjectwater-
dc.subjectanimal experiment-
dc.subjectanimal tissue-
dc.subjectblood pressure regulation-
dc.subjectbody weight-
dc.subjectbrain third ventricle-
dc.subjectcannula-
dc.subjectcontrolled study-
dc.subjectenzyme activation-
dc.subjectfluid intake-
dc.subjectinhibition kinetics-
dc.subjectmale-
dc.subjectmean arterial pressure-
dc.subjectnitrergic nerve-
dc.subjectnonhuman-
dc.subjectpressor response-
dc.subjectrat-
dc.subjectrat strain-
dc.subjectsodium appetite-
dc.subjectsodium intake-
dc.subjectAnimalia-
dc.titleInfluence of arginine vasopressin receptor and nitric oxide on the water, sodium intake and arterial blood pressure induce by angiotensin injected into third ventricle of the brainen
dc.typeoutro-
dc.contributor.institutionUniversidade de Taubaté (UNITAU)-
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)-
dc.contributor.institutionUniversidade de São Paulo (USP)-
dc.description.affiliationDepartment of Exacts and Naturals Sciences, Uiara, Araraquara São Paulo-
dc.description.affiliationInstitute of Bioscience UNITAU, Taubaté, SP-
dc.description.affiliationDepartment of Physiology and Pathology School of Dentistry UNESP, 1680 Humaitá Street, Araraquara, SP 14801-903-
dc.description.affiliationDepartment of Surgery School of Medicine University of São Paulo, São Paulo-
dc.description.affiliationPublic Medical Hospital, São Paulo-
dc.description.affiliationUnespDepartment of Physiology and Pathology School of Dentistry UNESP, 1680 Humaitá Street, Araraquara, SP 14801-903-
dc.identifier.doi10.3923/jbs.2006.182.186-
dc.rights.accessRightsAcesso aberto-
dc.relation.ispartofJournal of Biological Sciences-
dc.identifier.scopus2-s2.0-33644513409-
Appears in Collections:Artigos, TCCs, Teses e Dissertações da Unesp

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