Mineralocorticoid Receptor Blockade in End-Stage Renal Disease

Mineralocorticoid Receptor Blockade in End-Stage Renal Disease Curr Hypertens Rep (2017) 19: 40 DOI 10.1007/s11906-017-0737-y ANTIHYPERTENSIVE AGENTS: MECHANISMS OF DRUG ACTION (M ERNST, SECTION EDITOR) 1 2,3 Radmila Lyubarova & Elvira O. Gosmanova Published online: 27 April 2017 Springer Science+Business Media New York 2017 Abstract consequence—were low with careful patient selection and Purpose of Review The purpose of this study was to summa- monitoring. rize recent findings about cardiovascular benefits and safety of . . aldosterone blockade in patients with end-stage renal disease Keywords End-stage renal disease Aldosterone (ESRD). Aldosterone blockade Mineralocorticoid receptor blockade Recent Findings It is now well recognized that aldosterone’s deleterious cardiovascular impact is not limited to its pressor effect arising from an increase in sodium reabsorption in the Introduction kidneys. Aldosterone has also been shown to increase blood pressure by a direct activation of the sympathetic nervous The paradigm describing the cardiovascular effects of aldoste- system, to cause endothelial and vascular smooth muscle cell rone is rapidly evolving. Historically, aldosterone was dysfunction, myocardial remodeling and fibrosis, and to have regarded as a mineralocorticoid hormone that is synthesized pro-arrhythmogenic actions in the heart. These unconvention- and released into the systemic circulation by the adrenal al extra-renal effects of aldosterone make its blockade feasible http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Current Hypertension Reports Springer Journals

Mineralocorticoid Receptor Blockade in End-Stage Renal Disease

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Publisher
Springer US
Copyright
Copyright © 2017 by Springer Science+Business Media New York (outside the USA)
Subject
Medicine & Public Health; Internal Medicine; Cardiology; Metabolic Diseases; Nephrology; Primary Care Medicine; General Practice / Family Medicine
ISSN
1522-6417
eISSN
1534-3111
D.O.I.
10.1007/s11906-017-0737-y
Publisher site
See Article on Publisher Site

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