Mineralocorticoid Receptor and Hypertension

Call for Papers

Aldosterone, through binding to mineralocorticoid receptor (MR, NR3C2), promotes renal sodium reabsorption and potassium secretion in epithelial cells, most notably in the kidney and colon. Aldosterone also plays important roles in nonepithelial cells, such as cardiac myocytes and vascular walls. Primary aldosteronism, which is defined as hypertension, high plasma aldosterone concentration, and suppressed plasma renin activity level, reveals higher prevalence of cardiovascular diseases than essential hypertension. Recent data also indicates that inappropriate levels of aldosterone, in the presence of moderate to high salt intake, result in significant tissue damage in nonepithelial cells, such as endothelial dysfunction, vascular inflammation, and myocardial fibrosis through MR activation. Three clinical trials, the randomized Aldactone Evaluation Study (RALES), Eplerenone Postacute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS), and Eplerenone in Mild Patients Hospitalization and Survival Study in Heart Failure (EMPHASIS-HF), shed new light on MR as an important pathogenic mediator of cardiac and vascular remodeling, because treatment with MR antagonist spironolactone or eplerenone was effective in significantly reducing the morbidity and mortality of patients with congestive heart failure. However, the underlying molecular mechanisms of the successful treatment with MR antagonist remain to be elucidated. We invite investigators to contribute original research articles as well as review articles. Potential topics include, but are not limited to:

• Mechanisms of MR activation
• MR activation in the kidney
• MR activation in the heart
• MR activation in the vasculature
• Animal models of aldosterone-induced tissue damage
• Efficacy of MR antagonist in hypertension

Before submission authors should carefully read over the journal's Author Guidelines, which are located at http://www.hindawi.com/journals/ije/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/ according to the following timetable:

Lead Guest Editor

• Hirotaka Shibata, Department of Internal Medicine, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan

Guest Editors

• Morag Young, Steroid Receptor Biology, Prince Henry's Institute of Medical Research, P.O. Box 5152, Clayton, VIC 03166, Australia
• Marc Lombes, INSERM U693, Faculté de Médecine Paris-SUD, 63 rue Gabriel Peri, Le Kremlin-Bicetre, 94276 Paris, France
• Anne M. Dorrance, Department of Pharmacology and Toxicology, Michigan State University, MI 48824, USA