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(Hypertension. 2008;51:161.)
© 2008 American Heart Association, Inc.

Brief Review

Aldosterone and Vascular Inflammation

From the Division of Clinical Pharmacology, Departments of Medicine and Pharmacology, Vanderbilt University School of Medicine, Nashville, Tenn.

Correspondence to Nancy J. Brown, Departments of Medicine and Pharmacology, 560 Robinson Research Building, Vanderbilt University School of Medicine, Nashville, TN 37232-6602. E-mail nancy.j.brown@vanderbilt.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Oxidative stress and inflammation contribute to increased cardiovascular morbidity and mortality associated with activation of the renin-angiotensin (Ang)-aldosterone system (RAAS). Studies in cultured cells in vitro and in rodent models in vivo demonstrate that aldosterone and/or mineralocorticoid receptor (MR) activation cause oxidative stress and vascular inflammation. Translational studies in humans suggest that endogenous aldosterone increases inflammatory biomarkers through an MR-dependent pathway. Clinical studies indicate that the prevalence of hyperaldosteronism may be increased in resistant hypertension,¹ that aldosterone concentrations "escape" to pretreatment levels during chronic treatment of congestive heart failure or hypertension with an Ang-converting enzyme (ACE) inhibitor or Ang receptor blocker,^2–4 and that MR antagonism decreases mortality in congestive heart failure.^5,6 This article reviews the current literature regarding mechanism(s) of aldosterone-induced vascular inflammation and its implications for the prevention of vascular injury in humans.

	Role of Inflammation in Atherosclerosis and Vascular Remodeling

 
Oxidative stress and inflammation play central roles in the pathogenesis of atherosclerosis.^7,8 Reactive oxygen species, including superoxide and hydrogen peroxide, modify vascular low-density lipoproteins to form oxidized low-density lipoproteins. Low-density lipoproteins stimulate endothelial cells to express leukocyte adhesion molecules, such as vascular cell adhesion molecule, leading to the recruitment of monocytes and T lymphocytes, which invade the intima. Monocyte-derived macrophages, rich in nicotinamide-adenine-dinucleotide phosphate (NADPH) oxidase, amplify the generation of reactant oxygen species. Macrophages take up oxidized low-density lipoproteins via scavenger receptors to become foam cells. T cells and macrophages within atherosclerotic lesions produce chemokines and cytokines resulting in the migration and proliferation of vascular smooth muscle cells (VSMCs) within the intima. VSMCs, in turn, promote . . . [Full Text of this Article]

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