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Trends Endocrinol Metab. 2016 Mar;27(3):123-131. doi: 10.1016/j.tem.2016.01.003. Epub 2016 Jan 20.

Local Control of Aldosterone Production and Primary Aldosteronism.

Author information

1
Institut de Pharmacologie Moléculaire et Cellulaire CNRS, 06560 Valbonne, France; NEOGENEX CNRS International Associated Laboratory, 06560 Valbonne, France; Université de Nice - Sophia Antipolis, 06560 Sophia Antipolis, France. Electronic address: ninino@ipmc.cnrs.fr.
2
Laboratoire de PhysioMédecine Moléculaire CNRS-UNS UMR 7370, 06108 Nice Cedex 2, France; Laboratories of Excellence, Ion Channel Science and Therapeutics, 06107 Nice, France.
3
INSERM, UMRS 970, Paris Cardiovascular Research Center, Paris, France; Université Paris Descartes, Sorbonne Paris Cité, Paris, France; Assistance Publique-Hôpitaux de Paris, Hôpital Européen Georges Pompidou, Service de Génétique, 75015 Paris, France.
4
Medical Cell Biology - University of Regensburg, 93053 Regensburg, Germany.

Abstract

Primary aldosteronism (PA) is caused by excessive production of aldosterone by the adrenal cortex and is determined by a benign aldosterone-producing adenoma (APA) in a significant proportion of cases. Local mechanisms, as opposed to circulatory ones, that control aldosterone production in the adrenal cortex are particularly relevant in the physiopathological setting and in the pathogenesis of PA. A breakthrough in our understanding of the pathogenetic mechanisms in APA has been the identification of somatic mutations in genes controlling membrane potential and intracellular calcium concentrations. However, recent data show that the processes of nodule formation and aldosterone hypersecretion can be dissociated in pathological adrenals and suggest a model envisaging different molecular events for the pathogenesis of APA.

KEYWORDS:

adrenal cortex; aldosterone; calcium; potassium channels

PMID:
26803728
DOI:
10.1016/j.tem.2016.01.003
[Indexed for MEDLINE]

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