dc.contributorUniversidade Estadual Paulista (Unesp)
dc.creatorSaad, Wilson Abrão [UNESP]
dc.creatorCamargo, Luiz Antonio de Arruda [UNESP]
dc.creatorRenzi, Antonio [UNESP]
dc.creatorMenani, José Vanderlei [UNESP]
dc.creatorSaad, Willian Abrão [UNESP]
dc.date2014-05-27T11:18:01Z
dc.date2014-05-27T11:18:01Z
dc.date1995-07-21
dc.date.accessioned2023-09-12T07:19:24Z
dc.date.available2023-09-12T07:19:24Z
dc.identifierhttp://dx.doi.org/10.1016/0304-3940(95)11751-H
dc.identifierNeuroscience Letters, v. 194, n. 3, p. 169-172, 1995.
dc.identifier0304-3940
dc.identifierhttp://hdl.handle.net/11449/130583
dc.identifier10.1016/0304-3940(95)11751-H
dc.identifierWOS:A1995RL70100006
dc.identifier2-s2.0-0028990139
dc.identifier6551236936295697
dc.identifier1023597870118105
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8779887
dc.descriptionTo 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.
dc.descriptionDepartment of Physiology School of Dentistry Paulista State University, 1680 Humaitá Street, Araraquara, SP 14801-903
dc.descriptionDepartment of Physiology School of Dentistry Paulista State University, 1680 Humaitá Street, Araraquara, SP 14801-903
dc.format169-172
dc.languageeng
dc.publisherElsevier B.V.
dc.relationNeuroscience Letters
dc.relation2.159
dc.relation0,946
dc.rightsAcesso restrito
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 II
dc.typeArtigo


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