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

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dc.contributor.authorDe Luca Jr., Laurival A. [UNESP]
dc.contributor.authorXu, Zhice [UNESP]
dc.contributor.authorSchoorlemmer, Guus H. M. [UNESP]
dc.contributor.authorThunhorst, Robert L. [UNESP]
dc.contributor.authorBeltz, Terry G. [UNESP]
dc.contributor.authorMenani, José V. [UNESP]
dc.contributor.authorJohnson, Alan Kim [UNESP]
dc.contributor.institutionUniversity of Iowa
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)
dc.date.accessioned2022-04-28T19:55:26Z
dc.date.available2022-04-28T19:55:26Z
dc.date.issued2002-01-01
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.affiliationDepartments of Psychology Pharmacology and Exercise Science Cardiovascular Center University of Iowa, Iowa City, IA 52242-1407
dc.description.affiliationDepartment of Physiology and Pathology School of Dentistry Paulista State University, Sao Paulo 14801-903
dc.description.affiliationDept. of Physiology and Pathology-School of Dentistry Paulista State Univ. (UNESP), Sao Paulo 14801-903
dc.description.affiliationUnespDepartment of Physiology and Pathology School of Dentistry Paulista State University, Sao Paulo 14801-903
dc.description.affiliationUnespDept. of Physiology and Pathology-School of Dentistry Paulista State Univ. (UNESP), Sao Paulo 14801-903
dc.identifierhttp://dx.doi.org/10.1152/ajpregu.00295.2000
dc.identifier.citationAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology, v. 282, n. 2 51-2, 2002.
dc.identifier.doi10.1152/ajpregu.00295.2000
dc.identifier.issn0363-6119
dc.identifier.scopus2-s2.0-0036081479
dc.identifier.urihttp://hdl.handle.net/11449/224233
dc.language.isoeng
dc.relation.ispartofAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
dc.sourceScopus
dc.subjectCircumventricular organs
dc.subjectDehydration
dc.subjectHypovolemia
dc.subjectSalt intake
dc.subjectThirst
dc.titleWater deprivation-induced sodium appetite: Humoral and cardiovascular mediators and immediate early genesen
dc.typeArtigo

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