Journal article
Despite increasing aldosterone, elevated potassium is not necessary for activating aldosterone‐sensitive HSD2 neurons or sodium appetite
Physiological reports, Vol.9(2), pp.e14714-n/a
01/2021
DOI: 10.14814/phy2.14714
PMID: 33463885
Abstract
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.
Details
- Title: Subtitle
- Despite increasing aldosterone, elevated potassium is not necessary for activating aldosterone‐sensitive HSD2 neurons or sodium appetite
- Creators
- Frederico S Fazan - Department of Neurology Iowa Neuroscience InstituteUniversity of Iowa Hospital and Clinics Iowa City Iowa USA, Department of Physiology and Pathology São Paulo State University Araraquara BrazilEduardo Colombari - Department of Physiology and Pathology São Paulo State University Araraquara BrazilArthur D Loewy - Department of Neuroscience Washington University School of Medicine in Saint Louis St Louis Missouri USAJoel C Geerling - Department of Neurology Iowa Neuroscience InstituteUniversity of Iowa Hospital and Clinics Iowa City Iowa USA
- Resource Type
- Journal article
- Publication Details
- Physiological reports, Vol.9(2), pp.e14714-n/a
- DOI
- 10.14814/phy2.14714
- PMID
- 33463885
- NLM abbreviation
- Physiol Rep
- eISSN
- 2051-817X
- Grant note
- DOI: 10.13039/100000065, name: National Institute of Neurological Disorders and Stroke, award: NS099425; DOI: 10.13039/100000968, name: American Heart Association, award: 0510050Z; DOI: 10.13039/100000050, name: National Heart, Lung, and Blood Institute, award: HL25449; DOI: 10.13039/501100001807, name: Fundação de Amparo à Pesquisa do Estado de São Paulo, award: 2019/09820‐7
- Language
- English
- Date published
- 01/2021
- Academic Unit
- Neurology; Iowa Neuroscience Institute
- Record Identifier
- 9984070797102771
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