Signal Transduction of Mineralocorticoid and Angiotensin II Receptors in the Central Control of Sodium Appetite: A Narrative Review.

aldosterone angiotensin II mesolimbic dopaminergic system organum vasculosum lamina terminalis oxytocin paraventricular nucleus sodium appetite

Journal

International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791

Informations de publication

Date de publication:
29 Oct 2021
Historique:
received: 29 09 2021
revised: 16 10 2021
accepted: 25 10 2021
entrez: 13 11 2021
pubmed: 14 11 2021
medline: 15 12 2021
Statut: epublish

Résumé

Sodium appetite is an innate behavior occurring in response to sodium depletion that induces homeostatic responses such as the secretion of the mineralocorticoid hormone aldosterone from the zona glomerulosa of the adrenal cortex and the stimulation of the peptide hormone angiotensin II (ANG II). The synergistic action of these hormones signals to the brain the sodium appetite that represents the increased palatability for salt intake. This narrative review summarizes the main data dealing with the role of mineralocorticoid and ANG II receptors in the central control of sodium appetite. Appropriate keywords and MeSH terms were identified and searched in PubMed. References to original articles and reviews were examined, selected, and discussed. Several brain areas control sodium appetite, including the nucleus of the solitary tract, which contains aldosterone-sensitive HSD2 neurons, and the organum vasculosum lamina terminalis (OVLT) that contains ANG II-sensitive neurons. Furthermore, sodium appetite is under the control of signaling proteins such as mitogen-activated protein kinase (MAPK) and inositol 1,4,5-thriphosphate (IP3). ANG II stimulates salt intake via MAPK, while combined ANG II and aldosterone action induce sodium intake via the IP3 signaling pathway. Finally, aldosterone and ANG II stimulate OVLT neurons and suppress oxytocin secretion inhibiting the neuronal activity of the paraventricular nucleus, thus disinhibiting the OVLT activity to aldosterone and ANG II stimulation.

Identifiants

pubmed: 34769164
pii: ijms222111735
doi: 10.3390/ijms222111735
pmc: PMC8584094
pii:
doi:

Substances chimiques

Receptors, Angiotensin 0
Receptors, Mineralocorticoid 0
Sodium, Dietary 0
Angiotensin II 11128-99-7

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

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Auteurs

Michele Iovino (M)

Interdisciplinary Department of Medicine, Section of Internal Medicine, Geriatrics, Endocrinology and Rare Disease, University of Bari "Aldo Moro" School of Medicine, 70123 Bari, Italy.

Tullio Messana (T)

IRCCS, Istituto delle Scienze Neurologiche di Bologna, UOC of Pediatric Neuropsychiatry, 40139 Bologna, Italy.

Giuseppe Lisco (G)

Interdisciplinary Department of Medicine, Section of Internal Medicine, Geriatrics, Endocrinology and Rare Disease, University of Bari "Aldo Moro" School of Medicine, 70123 Bari, Italy.

Aldo Vanacore (A)

Interdisciplinary Department of Medicine, Section of Internal Medicine, Geriatrics, Endocrinology and Rare Disease, University of Bari "Aldo Moro" School of Medicine, 70123 Bari, Italy.

Vito Angelo Giagulli (VA)

Interdisciplinary Department of Medicine, Section of Internal Medicine, Geriatrics, Endocrinology and Rare Disease, University of Bari "Aldo Moro" School of Medicine, 70123 Bari, Italy.

Edoardo Guastamacchia (E)

Interdisciplinary Department of Medicine, Section of Internal Medicine, Geriatrics, Endocrinology and Rare Disease, University of Bari "Aldo Moro" School of Medicine, 70123 Bari, Italy.

Giovanni De Pergola (G)

Unit of Geriatrics and Internal Medicine, National Institute of Gastroenterology "Saverio de Bellis", Research Hospital, Castellana Grotte, 70124 Bari, Italy.

Vincenzo Triggiani (V)

Interdisciplinary Department of Medicine, Section of Internal Medicine, Geriatrics, Endocrinology and Rare Disease, University of Bari "Aldo Moro" School of Medicine, 70123 Bari, Italy.

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Classifications MeSH