Despite increasing aldosterone, elevated potassium is not necessary for activating aldosterone-sensitive HSD2 neurons or sodium appetite
Autor(a) principal: | |
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Data de Publicação: | 2021 |
Outros Autores: | , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNESP |
Texto Completo: | http://dx.doi.org/10.14814/phy2.14714 http://hdl.handle.net/11449/209997 |
Resumo: | Restricting dietary sodium promotes sodium appetite in rats. Prolonged sodium restriction increases plasma potassium (pK), and elevated pK is largely responsible for a concurrent increase in aldosterone, which helps promote sodium appetite. In addition to increasing aldosterone, we hypothesized that elevated potassium directly influences the brain to promote sodium appetite. To test this, we restricted dietary potassium in sodium-deprived rats. Potassium restriction reduced pK and blunted the increase in aldosterone caused by sodium deprivation, but did not prevent sodium appetite or the activation of aldosterone-sensitive HSD2 neurons. Conversely, supplementing potassium in sodium-deprived rats increased pK and aldosterone, but did not increase sodium appetite or the activation of HSD2 neurons relative to potassium restriction. Supplementing potassium without sodium deprivation did not significantly increase aldosterone and HSD2 neuronal activation and only modestly increased saline intake. Overall, restricting dietary sodium activated the HSD2 neurons and promoted sodium appetite across a wide range of pK and aldosterone, and saline consumption inactivated the HSD2 neurons despite persistent hyperaldosteronism. In conclusion, elevated potassium is important for increasing aldosterone, but it is neither necessary nor sufficient for activating HSD2 neurons and increasing sodium appetite. |
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Despite increasing aldosterone, elevated potassium is not necessary for activating aldosterone-sensitive HSD2 neurons or sodium appetitealdosteronedietary sodiummineralocorticoidpotassiumsalt appetitesalt hungerRestricting dietary sodium promotes sodium appetite in rats. Prolonged sodium restriction increases plasma potassium (pK), and elevated pK is largely responsible for a concurrent increase in aldosterone, which helps promote sodium appetite. In addition to increasing aldosterone, we hypothesized that elevated potassium directly influences the brain to promote sodium appetite. To test this, we restricted dietary potassium in sodium-deprived rats. Potassium restriction reduced pK and blunted the increase in aldosterone caused by sodium deprivation, but did not prevent sodium appetite or the activation of aldosterone-sensitive HSD2 neurons. Conversely, supplementing potassium in sodium-deprived rats increased pK and aldosterone, but did not increase sodium appetite or the activation of HSD2 neurons relative to potassium restriction. Supplementing potassium without sodium deprivation did not significantly increase aldosterone and HSD2 neuronal activation and only modestly increased saline intake. Overall, restricting dietary sodium activated the HSD2 neurons and promoted sodium appetite across a wide range of pK and aldosterone, and saline consumption inactivated the HSD2 neurons despite persistent hyperaldosteronism. In conclusion, elevated potassium is important for increasing aldosterone, but it is neither necessary nor sufficient for activating HSD2 neurons and increasing sodium appetite.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)American Heart AssociationNational Institutes of Heart, Lung, and Blood DisordersNational Institutes of Neurologic Disorders and StrokeUniv Iowa Hosp & Clin, Dept Neurol, Iowa Neurosci Inst, Iowa City, IA 52242 USASao Paulo State Univ, Dept Physiol & Pathol, Araraquara, SP, BrazilWashington Univ, Dept Neurosci, Sch Med St Louis, St Louis, MO 63110 USASao Paulo State Univ, Dept Physiol & Pathol, Araraquara, SP, BrazilFAPESP: 2019/09820-7American Heart Association: 0510050ZNational Institutes of Heart, Lung, and Blood Disorders: HL25449National Institutes of Neurologic Disorders and Stroke: NS099425Wiley-BlackwellUniv Iowa Hosp & ClinUniversidade Estadual Paulista (Unesp)Washington UnivFazan, Frederico S. [UNESP]Colombari, Eduardo [UNESP]Loewy, Arthur D.Geerling, Joel C.2021-06-25T12:36:12Z2021-06-25T12:36:12Z2021-01-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article11http://dx.doi.org/10.14814/phy2.14714Physiological Reports. Hoboken: Wiley, v. 9, n. 2, 11 p., 2021.2051-817Xhttp://hdl.handle.net/11449/20999710.14814/phy2.14714WOS:000614055200001Web of Sciencereponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengPhysiological Reportsinfo:eu-repo/semantics/openAccess2021-10-23T19:50:13Zoai:repositorio.unesp.br:11449/209997Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462021-10-23T19:50:13Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false |
dc.title.none.fl_str_mv |
Despite increasing aldosterone, elevated potassium is not necessary for activating aldosterone-sensitive HSD2 neurons or sodium appetite |
title |
Despite increasing aldosterone, elevated potassium is not necessary for activating aldosterone-sensitive HSD2 neurons or sodium appetite |
spellingShingle |
Despite increasing aldosterone, elevated potassium is not necessary for activating aldosterone-sensitive HSD2 neurons or sodium appetite Fazan, Frederico S. [UNESP] aldosterone dietary sodium mineralocorticoid potassium salt appetite salt hunger |
title_short |
Despite increasing aldosterone, elevated potassium is not necessary for activating aldosterone-sensitive HSD2 neurons or sodium appetite |
title_full |
Despite increasing aldosterone, elevated potassium is not necessary for activating aldosterone-sensitive HSD2 neurons or sodium appetite |
title_fullStr |
Despite increasing aldosterone, elevated potassium is not necessary for activating aldosterone-sensitive HSD2 neurons or sodium appetite |
title_full_unstemmed |
Despite increasing aldosterone, elevated potassium is not necessary for activating aldosterone-sensitive HSD2 neurons or sodium appetite |
title_sort |
Despite increasing aldosterone, elevated potassium is not necessary for activating aldosterone-sensitive HSD2 neurons or sodium appetite |
author |
Fazan, Frederico S. [UNESP] |
author_facet |
Fazan, Frederico S. [UNESP] Colombari, Eduardo [UNESP] Loewy, Arthur D. Geerling, Joel C. |
author_role |
author |
author2 |
Colombari, Eduardo [UNESP] Loewy, Arthur D. Geerling, Joel C. |
author2_role |
author author author |
dc.contributor.none.fl_str_mv |
Univ Iowa Hosp & Clin Universidade Estadual Paulista (Unesp) Washington Univ |
dc.contributor.author.fl_str_mv |
Fazan, Frederico S. [UNESP] Colombari, Eduardo [UNESP] Loewy, Arthur D. Geerling, Joel C. |
dc.subject.por.fl_str_mv |
aldosterone dietary sodium mineralocorticoid potassium salt appetite salt hunger |
topic |
aldosterone dietary sodium mineralocorticoid potassium salt appetite salt hunger |
description |
Restricting dietary sodium promotes sodium appetite in rats. Prolonged sodium restriction increases plasma potassium (pK), and elevated pK is largely responsible for a concurrent increase in aldosterone, which helps promote sodium appetite. In addition to increasing aldosterone, we hypothesized that elevated potassium directly influences the brain to promote sodium appetite. To test this, we restricted dietary potassium in sodium-deprived rats. Potassium restriction reduced pK and blunted the increase in aldosterone caused by sodium deprivation, but did not prevent sodium appetite or the activation of aldosterone-sensitive HSD2 neurons. Conversely, supplementing potassium in sodium-deprived rats increased pK and aldosterone, but did not increase sodium appetite or the activation of HSD2 neurons relative to potassium restriction. Supplementing potassium without sodium deprivation did not significantly increase aldosterone and HSD2 neuronal activation and only modestly increased saline intake. Overall, restricting dietary sodium activated the HSD2 neurons and promoted sodium appetite across a wide range of pK and aldosterone, and saline consumption inactivated the HSD2 neurons despite persistent hyperaldosteronism. In conclusion, elevated potassium is important for increasing aldosterone, but it is neither necessary nor sufficient for activating HSD2 neurons and increasing sodium appetite. |
publishDate |
2021 |
dc.date.none.fl_str_mv |
2021-06-25T12:36:12Z 2021-06-25T12:36:12Z 2021-01-01 |
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://dx.doi.org/10.14814/phy2.14714 Physiological Reports. Hoboken: Wiley, v. 9, n. 2, 11 p., 2021. 2051-817X http://hdl.handle.net/11449/209997 10.14814/phy2.14714 WOS:000614055200001 |
url |
http://dx.doi.org/10.14814/phy2.14714 http://hdl.handle.net/11449/209997 |
identifier_str_mv |
Physiological Reports. Hoboken: Wiley, v. 9, n. 2, 11 p., 2021. 2051-817X 10.14814/phy2.14714 WOS:000614055200001 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Physiological Reports |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
11 |
dc.publisher.none.fl_str_mv |
Wiley-Blackwell |
publisher.none.fl_str_mv |
Wiley-Blackwell |
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 |
|
_version_ |
1799964839555104768 |