Document Detail

Effects of aldosterone and mineralocorticoid receptor antagonism on cardiac ion channels in the view of upstream therapy of atrial fibrillation.
MedLine Citation:
PMID:  21460407     Owner:  NLM     Status:  In-Data-Review    
Abstract. Atrial fibrillation (AF) is the most common sustained arrhythmia in man. Over the past years, importance of the renin-angiotensin-aldosterone system in AF pathophysiology has been recognized. Lately, the role of aldosterone in AF pathophysiology and mineralocorticoid receptor (MR) antagonism in "upstream" AF treatment is discussed with special regards concerning the effects on AF-induced structural remodeling. However, there is more and more evidence that MR antagonism also influences atrial electrophysiology and, respectively, AF-induced electrical remodeling, whereas the molecular mechanisms are almost unknown. The aim of this mini-review is to give an overview about the role of aldosterone in AF pathophysiology in principle and to summarize current available data concerning affection of cardiac ion channels by aldosterone and MR antagonism. Finally, as modulation of oxidative stress is discussed as one main therapy principle of "upstream" treatment of AF, potential mechanisms how modulation of oxidative stress by aldosterone and accordingly MR antagonism might alter atrial ion currents are delineated. Summarized, publications concerning potential mechanisms of aldosterone- and MR antagonism-modulated cardiac ion channels in various experimental settings are almost exclusively limited to the ventricular level and, partly, they are also contradictorily. Translation of these data to the atria is problematic because atrial and ventricular electrophysiology exhibit remarkable differences. It can be concluded that further research on the "atrial level" is needed in order to clarify the potential impact of the affection of atrial ion channels by aldosterone and accordingly MR antagonism in "upstream" therapy of AF.
Roman Laszlo; Kerstin Bentz; Juergen Schreieck
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  General physiology and biophysics     Volume:  30     ISSN:  0231-5882     ISO Abbreviation:  Gen. Physiol. Biophys.     Publication Date:  2011 Mar 
Date Detail:
Created Date:  2011-04-04     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8400604     Medline TA:  Gen Physiol Biophys     Country:  Slovakia    
Other Details:
Languages:  eng     Pagination:  11-9     Citation Subset:  IM    
Medizinische Klinik III, Kardiologie und Kreislauferkrankungen, Eberhard Karls Universität Tuebingen, Otfried-Mueller-Strasse 10, D 72076 Tuebingen, Germany.
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