dc.contributorUniversidade Estadual Paulista (UNESP)
dc.creatorAndrade, Carina Aparecida Fabricio de
dc.creatorAndrade-Franzé, Glaucia Maria Fabricio de
dc.creatorDe Paula, PatrÍcia M.
dc.creatorLuca Júnior, Laurival Antonio De
dc.creatorMenani, José V.
dc.date2016-01-28T16:55:49Z
dc.date2016-10-25T21:28:27Z
dc.date2016-01-28T16:55:49Z
dc.date2016-10-25T21:28:27Z
dc.date2014
dc.date.accessioned2017-04-06T09:49:01Z
dc.date.available2017-04-06T09:49:01Z
dc.identifierBrazilian journal of medical and biological research, v. 47, n. 1, p. 11-18, 2014.
dc.identifier1414-431X
dc.identifierhttp://hdl.handle.net/11449/133605
dc.identifierhttp://acervodigital.unesp.br/handle/11449/133605
dc.identifier10.1590/1414-431X20133308
dc.identifierS0100-879X2014000100011
dc.identifierISSN1414-431X-2014-47-01-11-18.pdf
dc.identifier339253755971890
dc.identifierhttp://dx.doi.org/10.1590/1414-431X20133308
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/944135
dc.descriptionCentral α2-adrenoceptors and the pontine lateral parabrachial nucleus (LPBN) are involved in the control of sodium and water intake. Bilateral injections of moxonidine (α2-adrenergic/imidazoline receptor agonist) or noradrenaline into the LPBN strongly increases 0.3 M NaCl intake induced by a combined treatment of furosemide plus captopril. Injection of moxonidine into the LPBN also increases hypertonic NaCl and water intake and reduces oxytocin secretion, urinary sodium, and water excreted by cell-dehydrated rats, causing a positive sodium and water balance, which suggests that moxonidine injected into the LPBN deactivates mechanisms that restrain body fluid volume expansion. Pretreatment with specific α2-adrenoceptor antagonists injected into the LPBN abolishes the behavioral and renal effects of moxonidine or noradrenaline injected into the same area, suggesting that these effects depend on activation of LPBN α2-adrenoceptors. In fluid-depleted rats, the palatability of sodium is reduced by ingestion of hypertonic NaCl, limiting intake. However, in rats treated with moxonidine injected into the LPBN, the NaCl palatability remains high, even after ingestion of significant amounts of 0.3 M NaCl. The changes in behavioral and renal responses produced by activation of α2-adrenoceptors in the LPBN are probably a consequence of reduction of oxytocin secretion and blockade of inhibitory signals that affect sodium palatability. In this review, a model is proposed to show how activation of α2-adrenoceptors in the LPBN may affect palatability and, consequently, ingestion of sodium as well as renal sodium excretion.
dc.languageeng
dc.publisherBraz J Med Biol Res
dc.relationBrazilian journal of medical and biological research
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectParabrachial nucleus
dc.subjectSodium
dc.subjectNatriuresis
dc.subjectThirst
dc.subjectHindbrain
dc.subjectTaste
dc.titleRole of alfa2-adrenoceptors in the lateral parabrachial nucleus in the control of body fluid homeostasis
dc.typeOtro


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