Water deprivation-induced sodium appetite: humoral and cardiovascular mediators and immediate early genes

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dc.contributor.authorDe Luca, L. A.
dc.contributor.authorXu, Z. C.
dc.contributor.authorSchoorlemmer, GHM
dc.contributor.authorThunhorst, R. L.
dc.contributor.authorBeltz, T. G.
dc.contributor.authorMenani, José Vanderlei [UNESP]
dc.contributor.authorJohnson, A. K.
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionUniv Iowa
dc.date.accessioned2014-05-20T13:45:48Z
dc.date.available2014-05-20T13:45:48Z
dc.date.issued2002-02-01
dc.description.abstractAdult rats deprived of water for 24-30 h were allowed to rehydrate by ingesting only water for 1-2 h. Rats were then given access to both water and 1.8% NaCl. This procedure induced a sodium appetite defined by the operational criteria of a significant increase in 1.8% NaCl intake (3.8 +/- 0.8 ml/2 h; n = 6). Expression of Fos (as assessed by immunohistochemistry) was increased in the organum vasculosum of the lamina terminalis (OVLT), median preoptic nucleus (MnPO), subfornical organ (SFO), and supraoptic nucleus (SON) after water deprivation. After rehydration with water but before consumption of 1.8% NaCl, Fos expression in the SON disappeared and was partially reduced in the OVLT and MnPO. However, Fos expression did not change in the SFO. Water deprivation also 1) increased plasma renin activity (PRA), osmolality, and plasma Na+; 2) decreased blood volume; and 3) reduced total body Na+; but 4) did not alter arterial blood pressure. Rehydration with water alone caused only plasma osmolality and plasma Na+ concentration to revert to euhydrated levels. The changes in Fos expression and PRA are consistent with a proposed role for ANG II in the control of the sodium appetite produced by water deprivation followed by rehydration with only water.en
dc.description.affiliationUNESP, Paulista State Univ, Sch Dent, Dept Physiol & Pathol, BR-14801903 São Paulo, Araraquara, Brazil
dc.description.affiliationUniv Iowa, Coll Med, Dept Psychol, Iowa City, IA 52242 USA
dc.description.affiliationUniv Iowa, Coll Med, Dept Pharmacol, Iowa City, IA 52242 USA
dc.description.affiliationUniv Iowa, Coll Med, Dept Exercise Sci, Iowa City, IA 52242 USA
dc.description.affiliationUniv Iowa, Coll Med, Ctr Cardiovasc, Iowa City, IA 52242 USA
dc.description.affiliationUnespUNESP, Paulista State Univ, Sch Dent, Dept Physiol & Pathol, BR-14801903 São Paulo, Araraquara, Brazil
dc.format.extentR552-R559
dc.identifierhttp://ajpregu.physiology.org/content/282/2/R552
dc.identifier.citationAmerican Journal of Physiology-regulatory Integrative and Comparative Physiology. Bethesda: Amer Physiological Soc, v. 282, n. 2, p. R552-R559, 2002.
dc.identifier.issn0363-6119
dc.identifier.lattes1023597870118105
dc.identifier.urihttp://hdl.handle.net/11449/16149
dc.identifier.wosWOS:000173287100027
dc.language.isoeng
dc.publisherAmer Physiological Soc
dc.relation.ispartofAmerican Journal of Physiology: Regulatory Integrative and Comparative Physiology
dc.relation.ispartofjcr3.082
dc.relation.ispartofsjr1,550
dc.rights.accessRightsAcesso aberto
dc.sourceWeb of Science
dc.subjectsalt intakept
dc.subjecthypovolemiapt
dc.subjectcircumventricular organspt
dc.subjectdehydrationpt
dc.subjectthirstpt
dc.titleWater deprivation-induced sodium appetite: humoral and cardiovascular mediators and immediate early genesen
dc.typeArtigo
dcterms.licensehttp://www.the-aps.org/mm/Publications/Info-For-Authors/Copyright
dcterms.rightsHolderAmer Physiological Soc
unesp.author.lattes1023597870118105
unesp.author.orcid0000-0003-1167-4441[6]
unesp.author.orcid0000-0001-8270-2652[1]
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Odontologia, Araraquarapt

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