Hindbrain serotonin and the rapid induction of sodium appetite

Detalhes bibliográficos
Autor(a) principal: Menani, José Vanderlei [UNESP]
Data de Publicação: 2000
Outros Autores: De Luca, L. A., Thunhorst, R. L., Johnson, A. K.
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNESP
Texto Completo: http://ajpregu.physiology.org/content/279/1/R126
http://hdl.handle.net/11449/39505
Resumo: Both systemically administered furosemide and isoproterenol produce water intake (i.e., thirst). Curiously, however, in light of the endocrine and hemodynamic effects produced by these treatments, they are remarkably ineffective in eliciting intake of hypertonic saline solutions (i.e., operationally defined as sodium appetite). Recent work indicates that bilateral injections of the serotonin receptor antagonist methysergide into the lateral parabrachial nuclei (LPBN) markedly enhance a preexisting sodium appetite. The present studies establish that a de novo sodium appetite can be induced with LPBN-methysergide treatment under experimental conditions in which only water is typically ingested. The effects of bilateral LPBN injections of methysergide were studied on the intake of water and 0.3 M NaCl following acute (beginning 1 h after treatment) diuretic (furosemide)-induced sodium and water depletion and following subcutaneous isoproterenol treatment. With vehicle injected into the LPBN, furosemide treatment and isoproterenol injection both caused water drinking but essentially no intake of hypertonic saline. In contrast, bilateral treatment of the LPBN with methysergide induced the intake of 0.3 M NaCl after subcutaneous furosemide and isoproterenol. Water intake induced by subcutaneous furosemide or isoproterenol was not changed by LPBN-methysergide injections. The results indicate that blockade of LPBN-serotonin receptors produces a marked intake of hypertonic NaCl (i.e., a de novo sodium appetite) after furosemide treatment as well as subcutaneous isoproterenol.
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spelling Hindbrain serotonin and the rapid induction of sodium appetitefurosemidesodium intakewater intake5-hydroxytryptamineBoth systemically administered furosemide and isoproterenol produce water intake (i.e., thirst). Curiously, however, in light of the endocrine and hemodynamic effects produced by these treatments, they are remarkably ineffective in eliciting intake of hypertonic saline solutions (i.e., operationally defined as sodium appetite). Recent work indicates that bilateral injections of the serotonin receptor antagonist methysergide into the lateral parabrachial nuclei (LPBN) markedly enhance a preexisting sodium appetite. The present studies establish that a de novo sodium appetite can be induced with LPBN-methysergide treatment under experimental conditions in which only water is typically ingested. The effects of bilateral LPBN injections of methysergide were studied on the intake of water and 0.3 M NaCl following acute (beginning 1 h after treatment) diuretic (furosemide)-induced sodium and water depletion and following subcutaneous isoproterenol treatment. With vehicle injected into the LPBN, furosemide treatment and isoproterenol injection both caused water drinking but essentially no intake of hypertonic saline. In contrast, bilateral treatment of the LPBN with methysergide induced the intake of 0.3 M NaCl after subcutaneous furosemide and isoproterenol. Water intake induced by subcutaneous furosemide or isoproterenol was not changed by LPBN-methysergide injections. The results indicate that blockade of LPBN-serotonin receptors produces a marked intake of hypertonic NaCl (i.e., a de novo sodium appetite) after furosemide treatment as well as subcutaneous isoproterenol.Univ Iowa, Dept Psychol, Iowa City, IA 52242 USAUniv Iowa, Dept Pharmacol, Iowa City, IA 52242 USAUniv Iowa, Ctr Cardiovasc, Iowa City, IA 52242 USAPaulista State Univ, Sch Dent, Dept Physiol, BR-14801903 São Paulo, BrazilPaulista State Univ, Sch Dent, Dept Physiol, BR-14801903 São Paulo, BrazilAmer Physiological SocUniv IowaUniversidade Estadual Paulista (Unesp)Menani, José Vanderlei [UNESP]De Luca, L. A.Thunhorst, R. L.Johnson, A. K.2014-05-20T15:30:03Z2014-05-20T15:30:03Z2000-07-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleR126-R131http://ajpregu.physiology.org/content/279/1/R126American Journal of Physiology-regulatory Integrative and Comparative Physiology. Bethesda: Amer Physiological Soc, v. 279, n. 1, p. R126-R131, 2000.0363-6119http://hdl.handle.net/11449/39505WOS:0000881714000171023597870118105Web of Sciencereponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengAmerican Journal of Physiology: Regulatory Integrative and Comparative Physiology3.0821,550info:eu-repo/semantics/openAccess2021-10-23T10:45:21Zoai:repositorio.unesp.br:11449/39505Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462021-10-23T10:45:21Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false
dc.title.none.fl_str_mv Hindbrain serotonin and the rapid induction of sodium appetite
title Hindbrain serotonin and the rapid induction of sodium appetite
spellingShingle Hindbrain serotonin and the rapid induction of sodium appetite
Menani, José Vanderlei [UNESP]
furosemide
sodium intake
water intake
5-hydroxytryptamine
title_short Hindbrain serotonin and the rapid induction of sodium appetite
title_full Hindbrain serotonin and the rapid induction of sodium appetite
title_fullStr Hindbrain serotonin and the rapid induction of sodium appetite
title_full_unstemmed Hindbrain serotonin and the rapid induction of sodium appetite
title_sort Hindbrain serotonin and the rapid induction of sodium appetite
author Menani, José Vanderlei [UNESP]
author_facet Menani, José Vanderlei [UNESP]
De Luca, L. A.
Thunhorst, R. L.
Johnson, A. K.
author_role author
author2 De Luca, L. A.
Thunhorst, R. L.
Johnson, A. K.
author2_role author
author
author
dc.contributor.none.fl_str_mv Univ Iowa
Universidade Estadual Paulista (Unesp)
dc.contributor.author.fl_str_mv Menani, José Vanderlei [UNESP]
De Luca, L. A.
Thunhorst, R. L.
Johnson, A. K.
dc.subject.por.fl_str_mv furosemide
sodium intake
water intake
5-hydroxytryptamine
topic furosemide
sodium intake
water intake
5-hydroxytryptamine
description Both systemically administered furosemide and isoproterenol produce water intake (i.e., thirst). Curiously, however, in light of the endocrine and hemodynamic effects produced by these treatments, they are remarkably ineffective in eliciting intake of hypertonic saline solutions (i.e., operationally defined as sodium appetite). Recent work indicates that bilateral injections of the serotonin receptor antagonist methysergide into the lateral parabrachial nuclei (LPBN) markedly enhance a preexisting sodium appetite. The present studies establish that a de novo sodium appetite can be induced with LPBN-methysergide treatment under experimental conditions in which only water is typically ingested. The effects of bilateral LPBN injections of methysergide were studied on the intake of water and 0.3 M NaCl following acute (beginning 1 h after treatment) diuretic (furosemide)-induced sodium and water depletion and following subcutaneous isoproterenol treatment. With vehicle injected into the LPBN, furosemide treatment and isoproterenol injection both caused water drinking but essentially no intake of hypertonic saline. In contrast, bilateral treatment of the LPBN with methysergide induced the intake of 0.3 M NaCl after subcutaneous furosemide and isoproterenol. Water intake induced by subcutaneous furosemide or isoproterenol was not changed by LPBN-methysergide injections. The results indicate that blockade of LPBN-serotonin receptors produces a marked intake of hypertonic NaCl (i.e., a de novo sodium appetite) after furosemide treatment as well as subcutaneous isoproterenol.
publishDate 2000
dc.date.none.fl_str_mv 2000-07-01
2014-05-20T15:30:03Z
2014-05-20T15:30:03Z
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://ajpregu.physiology.org/content/279/1/R126
American Journal of Physiology-regulatory Integrative and Comparative Physiology. Bethesda: Amer Physiological Soc, v. 279, n. 1, p. R126-R131, 2000.
0363-6119
http://hdl.handle.net/11449/39505
WOS:000088171400017
1023597870118105
url http://ajpregu.physiology.org/content/279/1/R126
http://hdl.handle.net/11449/39505
identifier_str_mv American Journal of Physiology-regulatory Integrative and Comparative Physiology. Bethesda: Amer Physiological Soc, v. 279, n. 1, p. R126-R131, 2000.
0363-6119
WOS:000088171400017
1023597870118105
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv American Journal of Physiology: Regulatory Integrative and Comparative Physiology
3.082
1,550
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv R126-R131
dc.publisher.none.fl_str_mv Amer Physiological Soc
publisher.none.fl_str_mv Amer Physiological Soc
dc.source.none.fl_str_mv Web of Science
reponame:Repositório Institucional da UNESP
instname:Universidade Estadual Paulista (UNESP)
instacron:UNESP
instname_str Universidade Estadual Paulista (UNESP)
instacron_str UNESP
institution UNESP
reponame_str Repositório Institucional da UNESP
collection Repositório Institucional da UNESP
repository.name.fl_str_mv Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)
repository.mail.fl_str_mv
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