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Review

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

1
Interdisciplinary Department of Medicine, Section of Internal Medicine, Geriatrics, Endocrinology and Rare Disease, University of Bari “Aldo Moro” School of Medicine, 70123 Bari, Italy
2
IRCCS, Istituto delle Scienze Neurologiche di Bologna, UOC of Pediatric Neuropsychiatry, 40139 Bologna, Italy
3
Unit of Geriatrics and Internal Medicine, National Institute of Gastroenterology “Saverio de Bellis”, Research Hospital, Castellana Grotte, 70124 Bari, Italy
*
Author to whom correspondence should be addressed.
Academic Editor: Cristina Angeloni
Int. J. Mol. Sci. 2021, 22(21), 11735; https://doi.org/10.3390/ijms222111735
Received: 29 September 2021 / Revised: 16 October 2021 / Accepted: 25 October 2021 / Published: 29 October 2021
(This article belongs to the Special Issue Advances in Oxytocin)
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. View Full-Text
Keywords: sodium appetite; aldosterone; angiotensin II; organum vasculosum lamina terminalis; paraventricular nucleus; oxytocin; mesolimbic dopaminergic system sodium appetite; aldosterone; angiotensin II; organum vasculosum lamina terminalis; paraventricular nucleus; oxytocin; mesolimbic dopaminergic system
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MDPI and ACS Style

Iovino, M.; Messana, T.; Lisco, G.; Vanacore, A.; Giagulli, V.A.; Guastamacchia, E.; De Pergola, G.; Triggiani, V. Signal Transduction of Mineralocorticoid and Angiotensin II Receptors in the Central Control of Sodium Appetite: A Narrative Review. Int. J. Mol. Sci. 2021, 22, 11735. https://doi.org/10.3390/ijms222111735

AMA Style

Iovino M, Messana T, Lisco G, Vanacore A, Giagulli VA, Guastamacchia E, De Pergola G, Triggiani V. Signal Transduction of Mineralocorticoid and Angiotensin II Receptors in the Central Control of Sodium Appetite: A Narrative Review. International Journal of Molecular Sciences. 2021; 22(21):11735. https://doi.org/10.3390/ijms222111735

Chicago/Turabian Style

Iovino, Michele, Tullio Messana, Giuseppe Lisco, Aldo Vanacore, Vito Angelo Giagulli, Edoardo Guastamacchia, Giovanni De Pergola, and Vincenzo Triggiani. 2021. "Signal Transduction of Mineralocorticoid and Angiotensin II Receptors in the Central Control of Sodium Appetite: A Narrative Review" International Journal of Molecular Sciences 22, no. 21: 11735. https://doi.org/10.3390/ijms222111735

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