title: Regulation of aldosterone secretion: from physiology to disease.
abstract: Arterial hypertension is a major cardiovascular risk factor that affects between 10 and 40% of the population in industrialized countries. Primary aldosteronism (PA) is the most common form of secondary hypertension with an estimated prevalence of around 10% in referral centers and 4% in a primary care setting. Despite its high prevalence until recently, the underlying genetic and molecular basis of this common disease had remained largely obscure. Over the past decade, a number of insights have been achieved that have relied on in vitro cellular systems, wild-type and genetically modified in vivo models, as well as clinical studies in well-characterized patient populations. This progress has been made possible by a number of independent technical developments including that of specific hormone assays that allow measurement in small sample volumes as well as genetic techniques that enable high-throughput sequencing of a large number of samples. Furthermore, animal models have provided important insights into the physiology of aldosterone regulation that have served as a starting point for investigation of mechanisms involved in autonomous aldosterone secretion. Finally, national and international networks that have built up registries and biobanks have been instrumental in fostering translational research endeavors in PA. Therefore, it is to be expected that in the near future, further pathophysiological mechanisms that result in autonomous aldosterone secretion will be unraveled.
authors.affiliation: Endocrine Research Unit, Medizinische Klinik und Poliklinik IV, Klinikum der Universität München, Ziemssenstrasse 1, D-80336 Munich, Germany. felix.beuschlein@med.uni-muenchen.de
authors.forename: Felix
authors.initials: F
authors.lastname: Beuschlein
mesh_terms: D000236:Adenoma / Q000235:genetics; D000450:Aldosterone / Q000378:metabolism*; D000818:Animals; D051676:G Protein-Coupled Inwardly-Rectifying Potassium Channels / Q000235:genetics; D055106:Genome-Wide Association Study; D006801:Humans; D006929:Hyperaldosteronism / Q000235:genetics / Q000378:metabolism; D051379:Mice; D008954:Models, Biological; D000254:Sodium-Potassium-Exchanging ATPase / Q000235:genetics
chemical_list: D051676:G Protein-Coupled Inwardly-Rectifying Potassium Channels; C484274:KCNJ5 protein, human; D000450:Aldosterone; D000254:Sodium-Potassium-Exchanging ATPase