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Effects of systemic hyperkalemia: neural HSD2 activation and water balance

Grant number: 19/09820-7
Support Opportunities:Scholarships abroad - Research Internship - Master's degree
Effective date (Start): September 01, 2019
Effective date (End): February 29, 2020
Field of knowledge:Biological Sciences - Physiology - Physiology of Organs and Systems
Principal Investigator:Eduardo Colombari
Grantee:Frederico Sassoli Fazan
Supervisor: Joel C. Geerling
Host Institution: Faculdade de Odontologia (FOAr). Universidade Estadual Paulista (UNESP). Campus de Araraquara. Araraquara , SP, Brazil
Research place: University of Iowa, United States  
Associated to the scholarship:18/02194-0 - Role of central aldosterone in the neural control of renal function, BP.MS


Aldosterone is a mineralocorticoid produced by the suprarenal glands with several physiological functions including the modulation of blood pressure and the water-electrolyte content of the internal medium. The synthesis and release of aldosterone occur in the hypovolemic and especially in the hyperkalemic state. Aldosterone acts through interaction with the mineralocorticoid receptor (MR). These receptors also interact with great affinity to the glucocorticoid cortisol. In order to prevent unspecific MR binding, the aldosterone-sensitive cells express the enzyme 11²-hydroxysteroid dehydrogenase type 2 (HSD2) that is capable of converting cortisol into cortisone, leaving the MR prone to aldosterone binding. Recent studies have shown the presence of HSD2 cells in the nucleus of the solitary tract (NTS) in the central nervous system, suggesting aldosterone participation as a neuromodulator hormone. In fact, these HSD2 neurons are associated with sodium appetite by synergistic action of aldosterone and angiotensin II in the NTS. However, whether these cells are activated during hyperkalemic-induced hyperaldosteronism has not been studied. The aim of this study is to analyze the effects of hyperkalemia-induced secondary hyperaldosteronism in the HSD2 cells of the NTS. This research may reveal if these cells participate in the sensing or/and management of potassium internal or external balance and serve as a guide to further research in this topic. (AU)

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Scientific publications
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
FAZAN, FREDERICO S.; COLOMBARI, EDUARDO; LOEWY, ARTHUR D.; GEERLING, JOEL C.. Despite increasing aldosterone, elevated potassium is not necessary for activating aldosterone-sensitive HSD2 neurons or sodium appetite. PHYSIOLOGICAL REPORTS, v. 9, n. 2, . (19/09820-7)

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