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Current Hypertension Reports

Erschienen in:

01.06.2015 | Hypertension and the Kidney (RM Carey, Section Editor)

Activation of Mineralocorticoid Receptor in Salt-Sensitive Hypertension

verfasst von: Nobuhiro Ayuzawa, Toshiro Fujita

Erschienen in: Current Hypertension Reports | Ausgabe 6/2015

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Abstract

The impaired capacity of the kidney to excrete sodium plays an essential role in the development of hypertension. Adrenal corticosteroids control renal handling of sodium by regulating tubular sodium reabsorption in the distal nephron where both mineralocorticoid receptors (MR) and glucocorticoid receptors are expressed. In addition, cell type- and segment-specific expression of 11β-HSD2 and sodium transporters such as Na–Cl cotransporter (NCC), epithelial sodium channel (ENaC), and pendrin/Na⁺-driven Cl⁻/HCO₃ ⁻ exchanger (NDCBE) builds a distinctive model of sodium transport in the aldosterone-sensitive distal nephron. Aberrant MR activation in the distal nephron triggers salt-sensitive hypertension and hypokalemia through inappropriate sodium reabsorption and potassium secretion. However, MR activity is not necessarily modulated by the ligand alone. Recently, several lines of evidence revealed alternative mechanisms that regulate the activity of MR in a ligand-independent manner or through ligand binding modulation. This review summarizes the disorders related to MR activation in individual tubular cells and highlights the renal mechanism of salt-sensitive hypertension and new approaches for the prevention and treatment of this disease.

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Titel: Activation of Mineralocorticoid Receptor in Salt-Sensitive Hypertension
verfasst von: Nobuhiro Ayuzawa
Toshiro Fujita
Publikationsdatum: 01.06.2015
Verlag: Springer US
Erschienen in: Current Hypertension Reports / Ausgabe 6/2015
Print ISSN: 1522-6417
Elektronische ISSN: 1534-3111
DOI: https://doi.org/10.1007/s11906-015-0552-2

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