eplerenone has been researched along with Endomyocardial-Fibrosis* in 2 studies
1 review(s) available for eplerenone and Endomyocardial-Fibrosis
Article | Year |
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The role of aldosterone in heart failure and the clinical benefits of aldosterone blockade.
Aldosterone has a variety of detrimental effects on the heart and vasculature and is increasingly recognized as an important target in chronic heart failure, as illustrated by the Randomized Aldactone Evaluation Study. In this article, the evidence supporting the cardiovascular effects of aldosterone in humans and the proven benefits of aldosterone-receptor antagonists in heart failure shall be discussed. Topics: Aldosterone; Autonomic Nervous System Diseases; Endomyocardial Fibrosis; Eplerenone; Heart Failure; Humans; Mineralocorticoid Receptor Antagonists; Spironolactone; Vascular Diseases; Water-Electrolyte Imbalance | 2004 |
1 other study(ies) available for eplerenone and Endomyocardial-Fibrosis
Article | Year |
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Aldosterone induces a vascular inflammatory phenotype in the rat heart.
Vascular inflammation was examined as a potential mechanism of aldosterone-mediated myocardial injury in uninephrectomized rats receiving 1% NaCl-0.3% KCl to drink for 1, 2, or 4 wk and 1) vehicle, 2) aldosterone infusion (0.75 microg/h), or 3) aldosterone infusion (0.75 microg/h) plus the selective aldosterone blocker eplerenone (100 mg. kg(-1). day(-1)). Aldosterone induced severe hypertension at 4 wk [systolic blood pressure (SBP), 210 +/- 3 mmHg vs. vehicle, 131 +/- 2 mmHg, P < 0.001], which was partially attenuated by eplerenone (SBP, 180 +/- 7 mmHg; P < 0.001 vs. aldosterone alone and vehicle). No significant increases in myocardial interstitial collagen fraction or hydroxyproline concentration were detected throughout the study. However, histopathological analysis of the heart revealed severe coronary inflammatory lesions, which were characterized by monocyte/macrophage infiltration and resulted in focal ischemic and necrotic changes. The histological evidence of coronary lesions was preceded by and associated with the elevation of cyclooxygenase-2 (up to approximately 4-fold), macrophage chemoattractant protein-1 (up to approximately 4-fold), and osteopontin (up to approximately 13-fold) mRNA expression. Eplerenone attenuated proinflammatory molecule expression in the rat heart and subsequent vascular and myocardial damage. Thus aldosterone and salt treatment in uninephrectomized rats led to severe hypertension and the development of a vascular inflammatory phenotype in the heart, which may represent one mechanism by which aldosterone contributes to myocardial disease. Topics: Aldosterone; Animals; Blood Pressure; Chemokine CCL2; Coronary Vessels; Cyclooxygenase 2; Endomyocardial Fibrosis; Eplerenone; Gene Expression; Hypertension; Immunohistochemistry; In Situ Hybridization; Intercellular Adhesion Molecule-1; Isoenzymes; Male; Myocardium; Osteopontin; Phenotype; Prostaglandin-Endoperoxide Synthases; Rats; Rats, Sprague-Dawley; Sialoglycoproteins; Spironolactone; Vascular Cell Adhesion Molecule-1; Vasculitis | 2002 |