Hindbrain mineralocorticoid mechanisms on sodium appetite

dc.contributorUniversidade Estadual Paulista (UNESP)
dc.creatorColombari, Eduardo
dc.creatorFormenti, Silmara
dc.creatorBassi, Mirian
dc.creatorNakamura, Natália B.
dc.creatorSchoorlemmer, Guus H. M.
dc.creatorMenani, José Vanderlei
dc.date2014-05-27T11:28:20Z
dc.date2016-10-25T18:43:28Z
dc.date2014-05-27T11:28:20Z
dc.date2016-10-25T18:43:28Z
dc.date2013-02-01
dc.date.accessioned2017-04-06T02:12:22Z
dc.date.available2017-04-06T02:12:22Z
dc.identifierAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology, v. 304, n. 3, 2013.
dc.identifier0363-6119
dc.identifier1522-1490
dc.identifierhttp://hdl.handle.net/11449/74524
dc.identifierhttp://acervodigital.unesp.br/handle/11449/74524
dc.identifier10.1152/ajpregu.00385.2011
dc.identifierWOS:000314643400010
dc.identifier2-s2.0-84873297697
dc.identifierhttp://dx.doi.org/10.1152/ajpregu.00385.2011
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/895289
dc.descriptionAldosterone acting on the brain stimulates sodium appetite and sympathetic activity by mechanisms that are still not completely clear. In the present study, we investigated the effects of chronic infusion of aldosterone and acute injection of the mineralocorticoid receptor (MR) antagonist RU 28318 into the fourth ventricle (4th V) on sodium appetite. Male Wistar rats (280-350 g) with a stainless-steel cannula in either the 4th V or lateral ventricle (LV) were used. Daily intake of 0.3 M NaCl increased to 46 ± 15 and 130 ± 6 ml/24 h after 6 days of infusion of 10 and 100 ng/h of aldosterone into the 4th V (intake with vehicle infusion: 2 ± 1 ml/24 h). Water intake fell slightly and not consistently, and food intake was not affected by aldosterone. Sodium appetite induced by diuretic (furosemide) combined with 24 h of a low-sodium diet fell from 12 ± 1.7 ml/2 h to 5.6 ± 0.8 ml/2 h after injection of the MR antagonist RU 28318 (100 ng/2 μl) into the 4th V. RU 28318 also reduced the intake of 0.3 M NaCl induced by 9 days of a low-sodium diet from 9.5 ± 2.6 ml/2 h to 1.2 ± 0.6 ml/2 h. Infusion of 100 or 500 ng/h of aldosterone into the LV did not affect daily intake of 0.3 M NaCl. The results are functional evidence that aldosterone acting on MR in the hindbrain activates a powerful mechanism involved in the control of sodium appetite. © 2013 the American Physiological Society.
dc.languageeng
dc.relationAmerican Journal of Physiology: Regulatory Integrative and Comparative Physiology
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectAldosterone
dc.subjectMineralocorticoid receptor
dc.subjectRU 28318
dc.subjectSodium depletion
dc.subjectSodium ingestion
dc.subjectaldosterone
dc.subjectmineralocorticoid
dc.subjectmineralocorticoid receptor
dc.subjectoxprenoate potassium
dc.subjectsodium chloride
dc.subjectanimal cell
dc.subjectanimal experiment
dc.subjectanimal tissue
dc.subjectbrain ventricle
dc.subjectcontrolled study
dc.subjectmale
dc.subjectnonhuman
dc.subjectosmotic minipump
dc.subjectpriority journal
dc.subjectrat
dc.subjectrhombencephalon
dc.subjectsodium appetite
dc.subjectsodium restriction
dc.subjectAnimals
dc.subjectAppetite
dc.subjectEating
dc.subjectMale
dc.subjectMineralocorticoid Receptor Antagonists
dc.subjectMineralocorticoids
dc.subjectRats
dc.subjectRats, Wistar
dc.subjectRhombencephalon
dc.subjectSodium, Dietary
dc.titleHindbrain mineralocorticoid mechanisms on sodium appetite
dc.typeOtro


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