Abstract
Sodium appetite can be enhanced by the adrenal steroid aldosterone via an unknown brain mechanism. A novel group of neurons in the nucleus tractus solitarius expresses the enzyme 11-beta-hydroxysteroid dehydrogenase type 2, which makes them selectively responsive to aldosterone. Their activation parallels sodium appetite in different paradigms of salt loss even in the absence of aldosterone. These unique aldosterone target neurons may represent a previously unrecognized central convergence point at which hormonal and neural signals can be integrated to drive sodium appetite.
Publication types
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Comparative Study
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
MeSH terms
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11-beta-Hydroxysteroid Dehydrogenase Type 2 / analysis*
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11-beta-Hydroxysteroid Dehydrogenase Type 2 / physiology
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Adrenalectomy
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Aldosterone / administration & dosage
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Aldosterone / pharmacology
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Aldosterone / physiology*
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Animals
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Appetite / physiology*
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Corticosterone / administration & dosage
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Corticosterone / pharmacology
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Desoxycorticosterone / pharmacology
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Diet, Sodium-Restricted / adverse effects
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Diuresis / drug effects
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Furosemide / pharmacology
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Furosemide / toxicity
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Genes, fos
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Hyperaldosteronism / physiopathology
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Hyponatremia / etiology
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Hyponatremia / physiopathology*
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Infusion Pumps, Implantable
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Male
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Natriuresis / drug effects
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Neurons / classification
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Neurons / enzymology
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Neurons / physiology*
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Proto-Oncogene Proteins c-fos / biosynthesis
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Rats
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Rats, Sprague-Dawley
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Receptors, Mineralocorticoid / analysis*
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Receptors, Mineralocorticoid / physiology
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Sodium / deficiency*
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Sodium, Dietary* / administration & dosage
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Solitary Nucleus / physiology*
Substances
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Proto-Oncogene Proteins c-fos
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Receptors, Mineralocorticoid
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Sodium, Dietary
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Desoxycorticosterone
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Aldosterone
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Furosemide
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Sodium
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11-beta-Hydroxysteroid Dehydrogenase Type 2
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Corticosterone