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Please use this identifier to cite or link to this item: http://acervodigital.unesp.br/handle/11449/64222
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dc.contributor.authorHaibara, A. S.-
dc.contributor.authorSaad, W. A.-
dc.contributor.authorCamargo, L. A A-
dc.contributor.authorMenani, José Vanderlei-
dc.contributor.authorRenzi, Antonio-
dc.contributor.authorDe Luca, L. A.-
dc.contributor.authorAntunes-Rodrigues, J.-
dc.date.accessioned2014-05-27T11:17:28Z-
dc.date.accessioned2016-10-25T18:12:53Z-
dc.date.available2014-05-27T11:17:28Z-
dc.date.available2016-10-25T18:12:53Z-
dc.date.issued1992-02-01-
dc.identifierhttp://dx.doi.org/10.1016/0361-9230(92)90174-V-
dc.identifier.citationBrain Research Bulletin, v. 28, n. 2, p. 155-160, 1992.-
dc.identifier.issn0361-9230-
dc.identifier.urihttp://hdl.handle.net/11449/64222-
dc.identifier.urihttp://acervodigital.unesp.br/handle/11449/64222-
dc.description.abstractThe present study investigates the participation and interaction between cholinergic and opiate receptors of the medial septal area (MSA) in the regulation of Na+, K+ and water excretion, drinking and blood pressure regulation. Male Holtzman rats were implanted with stainless steel cannulae opening into the MSA. Na+, K+ and water excretion, water intake and blood pressure were measured after injection of carbachol (cholinergic agonist), FK-33824 (an opiate agonist) + carbachol or naloxone (an opiate antagonist) + carbachol into MSA. Carbachol (0.5 or 2.0 nmol) induced an increase in Na+ and K+ excretion, water intake and blood pressure and reduced the urinary volume. FK-33824 reduced the urinary volume and Na+ and K+ excretion. Previous injection of FK-33824 (100 ng) into the MSA blocked the increases in Na+ and K+ excretion, water intake and blood pressure induced by carbachol. Naloxone (10 μg) produced no changes in the effect of 2.0 nmol carbachol, but potentiated the natriuretic effect induced by 0.5 nmol dose of carbachol. These data show an inhibitory effect of opiate receptors on the changes in cardiovascular, fluid and electrolyte balance induced by cholinergic stimulation of the MSA in rats. © 1992.en
dc.format.extent155-160-
dc.language.isoeng-
dc.sourceScopus-
dc.subjectCarbacholl-
dc.subjectCardiovascular responses-
dc.subjectElectrolyte excretion-
dc.subjectOpiates-
dc.subjectSeptal area-
dc.subjectcarbachol-
dc.subjectcholinergic receptor stimulating agent-
dc.subjectenkephalin[2 dextro alanine 4 methylphenylalanine 5 methioninol sulfoxide]-
dc.subjectnaloxone-
dc.subjectopiate agonist-
dc.subjectopiate antagonist-
dc.subjectopiate receptor-
dc.subjectanimal experiment-
dc.subjectanimal tissue-
dc.subjectblood pressure-
dc.subjectcontrolled study-
dc.subjectdrinking-
dc.subjectelectrolyte excretion-
dc.subjectintracerebral drug administration-
dc.subjectmale-
dc.subjectnonhuman-
dc.subjectpriority journal-
dc.subjectrat-
dc.subjectseptum nucleus-
dc.subjectAnalysis of Variance-
dc.subjectAnimal-
dc.subjectBlood Pressure-
dc.subjectBrain-
dc.subjectCarbachol-
dc.subjectDiuresis-
dc.subjectDrinking Behavior-
dc.subjectDrug Interactions-
dc.subjectFK 33-824-
dc.subjectHeart Rate-
dc.subjectMale-
dc.subjectNaloxone-
dc.subjectNatriuresis-
dc.subjectRats-
dc.subjectReference Values-
dc.subjectSupport, Non-U.S. Gov't-
dc.titleOpiate activation suppresses the drinking, pressor and natriuretic responses induced by cholinergic stimulation of the medial septal areaen
dc.typeoutro-
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)-
dc.contributor.institutionUniversidade de São Paulo (USP)-
dc.description.affiliationDepartment of Physiological Sciences School of Dentistry UNESP, 14800 Araraquara, SP-
dc.description.affiliationDepartment of Physiology School of Medicine USP, 14049 Ribeirão Preto, SP-
dc.description.affiliationUnespDepartment of Physiological Sciences School of Dentistry UNESP, 14800 Araraquara, SP-
dc.identifier.doi10.1016/0361-9230(92)90174-V-
dc.rights.accessRightsAcesso restrito-
dc.relation.ispartofBrain Research Bulletin-
dc.identifier.scopus2-s2.0-0026500743-
Appears in Collections:Artigos, TCCs, Teses e Dissertações da Unesp

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