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Please use this identifier to cite or link to this item: http://acervodigital.unesp.br/handle/11449/130583
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dc.contributor.authorSaad, Wilson Abrão-
dc.contributor.authorCamargo, Luiz Antonio de Arruda-
dc.contributor.authorRenzi, Antonio-
dc.contributor.authorMenani, José Vanderlei-
dc.contributor.authorSaad, Willian Abrão-
dc.date.accessioned2014-05-27T11:18:01Z-
dc.date.accessioned2016-10-25T21:21:31Z-
dc.date.available2014-05-27T11:18:01Z-
dc.date.available2016-10-25T21:21:31Z-
dc.date.issued1995-07-21-
dc.identifierhttp://dx.doi.org/10.1016/0304-3940(95)11751-H-
dc.identifier.citationNeuroscience Letters, v. 194, n. 3, p. 169-172, 1995.-
dc.identifier.issn0304-3940-
dc.identifier.urihttp://hdl.handle.net/11449/130583-
dc.identifier.urihttp://acervodigital.unesp.br/handle/11449/130583-
dc.description.abstractTo determine whether central α1 and α2-adrenergic mechanisms are involved in urinary sodium and potassium excretion and urine volume induced by angiotensin II (ANGII), these renal parameters were measured in volume-expanded Holtzman rats with cannulas implanted into lateral ventricle (LV) and lateral hypothalamus (LH). The injection of ANGII into LV in rats with volume expansion reduced the sodium, potassium and urine excretion in comparison to the control injections of isotonic saline, whereas prazosin (α1 antagonist) potentiated these effects. Clonidine (α2 agonist) and yohimbine (α2 antagonist) injected into LH previous to injection of ANGII into LV also abolished the inhibitory effect of ANGII. These results suggest that the discharge of central alpha-adrenergic receptors has dual inhibitory and excitatory effect on antinatriuretic, antikaliuretic and antidiuretic effect induced by central ANGII in volume-expanded rats. © 1995.en
dc.format.extent169-172-
dc.language.isoeng-
dc.publisherElsevier B.V.-
dc.sourceScopus-
dc.subjectPotassium-
dc.subjectSodium-
dc.subjectUrinary volume-
dc.subjectAlpha 1 adrenergic receptor-
dc.subjectAlpha 1 adrenergic receptor blocking agent-
dc.subjectAlpha 2 adrenergic receptor-
dc.subjectAlpha 2 adrenergic receptor blocking agent-
dc.subjectAlpha 2 adrenergic receptor stimulating agent-
dc.subjectAlpha adrenergic receptor stimulating agent-
dc.subjectAngiotensin-
dc.subjectClonidine-
dc.subjectPotassium-
dc.subjectPrazosin-
dc.subjectSodium-
dc.subjectYohimbine-
dc.subjectAnimal experiment-
dc.subjectControlled study-
dc.subjectHypothalamus-
dc.subjectMale-
dc.subjectNonhuman-
dc.subjectPriority journal-
dc.subjectRat-
dc.subjectUrinary excretion-
dc.subjectAnimal-
dc.subjectDrug effect-
dc.subjectDrug interaction-
dc.subjectMetabolism-
dc.subjectMicturition-
dc.subjectRat strain-
dc.subjectAngiotensin II-
dc.subjectAnimal-
dc.subjectClonidine-
dc.subjectDrug Interactions-
dc.subjectHypothalamus-
dc.subjectMale-
dc.subjectPrazosin-
dc.subjectRats-
dc.subjectRats, Inbred Strains-
dc.subjectSupport, Non-U.S. Gov't-
dc.subjectUrination-
dc.subjectYohimbine-
dc.titleRole of alpha1 and alpha2-adrenoceptors of the lateral hypothalamic area on urinary excretion caused by centrally administered angiotensin IIen
dc.typeoutro-
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)-
dc.description.affiliationDepartment of Physiology School of Dentistry Paulista State University, 1680 Humaitá Street, Araraquara, SP 14801-903-
dc.description.affiliationUnespDepartment of Physiology School of Dentistry Paulista State University, 1680 Humaitá Street, Araraquara, SP 14801-903-
dc.identifier.doi10.1016/0304-3940(95)11751-H-
dc.identifier.wosWOS:A1995RL70100006-
dc.rights.accessRightsAcesso restrito-
dc.relation.ispartofNeuroscience Letters-
dc.identifier.scopus2-s2.0-0028990139-
Appears in Collections:Artigos, TCCs, Teses e Dissertações da Unesp

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