Molecular Mechanisms of Primary Aldosteronism
10.3803/EnM.2019.34.4.355
- Author:
Sergei G TEVOSIAN
1
;
Shawna C FOX
;
Hans K GHAYEE
Author Information
1. Department of Physiological Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL, USA.
- Publication Type:Review
- Keywords:
Hyperaldosteronism;
Hypertension;
Mineralocorticoids
- MeSH:
Adenoma;
Adrenal Cortex;
Aldosterone;
Cytokines;
Gene Expression Profiling;
Humans;
Hyperaldosteronism;
Hyperplasia;
Hypertension;
Mineralocorticoids;
Mortality;
Sirolimus
- From:Endocrinology and Metabolism
2019;34(4):355-366
- CountryRepublic of Korea
- Language:English
-
Abstract:
Primary aldosteronism (PA) results from excess production of mineralocorticoid hormone aldosterone by the adrenal cortex. It is normally caused either by unilateral aldosterone-producing adenoma (APA) or by bilateral aldosterone excess as a result of bilateral adrenal hyperplasia. PA is the most common cause of secondary hypertension and associated morbidity and mortality. While most cases of PA are sporadic, an important insight into this debilitating disease has been derived through investigating the familial forms of the disease that affect only a minor fraction of PA patients. The advent of gene expression profiling has shed light on the genes and intracellular signaling pathways that may play a role in the pathogenesis of these tumors. The genetic basis for several forms of familial PA has been uncovered in recent years although the list is likely to expand. Recently, the work from several laboratories provided evidence for the involvement of mammalian target of rapamycin pathway and inflammatory cytokines in APAs; however, their mechanism of action in tumor development and pathophysiology remains to be understood.
