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(Hypertension. 2008;51:624.)
© 2008 American Heart Association, Inc.

Editorial Commentaries

More NO-No More ROS

Combined Selective Mineralocorticoid Receptor Blockade and Angiotensin-Converting Enzyme Inhibition for Vascular Protection

Johann Bauersachs; Daniela Fraccarollo

From the Medizinische Klinik und Poliklinik I, Universitätsklinikum, Julius-Maximilians-Universität Würzburg, Würzburg, Germany.

Correspondence to Johann Bauersachs, Medizinische Klinik und Poliklinik I, Universitätsklinikum, Josef-Schneider-Str 2, D-97080 Würzburg, Germany. E-mail j.bauersachs@medizin.uni-wuerzburg.de

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

Angiotensin-converting enzyme (ACE) inhibitors significantly reduce cardiovascular events in patients with established or at high risk for coronary artery disease; however, the favorable effect appears to be modest.¹ Although early after initiation of therapy ACE inhibition reduces plasma levels of both angiotensin II and aldosterone, during prolonged ACE inhibition aldosterone levels may increase, the so-called aldosterone escape. Aldosterone levels independently predict cardiovascular risk,² and direct detrimental effects of aldosterone on the vascular wall have been described³: mineralocorticoid receptor (MR) activation stimulates the formation of reactive oxygen species (ROS) in endothelial cells and limits NO generation and bioavailability.⁴ Angiotensin II–mediated ROS formation in the vascular wall may be mediated in part by MR activation,⁵ and aldosterone potentiates angiotensin II–induced signaling processes in vascular smooth muscle cells.⁶ During inflammatory conditions, aldosterone and cortisol may act as agonists at the MR, thus leading to detrimental effects of MR activation, even in the absence of elevated concentrations of aldosterone.⁷

MR blockade reduces ROS formation and improves left ventricular remodeling, as well as endothelial function, when added to ACE inhibition in heart failure.⁸ Although eplerenone attenuated atherosclerosis in cholesterol-fed monkeys,⁹ it was unclear whether adding eplerenone to an ACE inhibitor would be more useful for preventing atherosclerosis progression than monotherapy with an ACE inhibitor.

In the present issue of Hypertension, Imanishi et al¹⁰ show the additional impact of eplerenone and ACE inhibition on atherosclerotic changes in genetically hyperlipidemic rabbits and dissected several potential underlying mechanisms. ACE inhibition and MR blockade displayed sustained vascular . . . [Full Text of this Article]

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Hypertension 2008 51: 734-741. [Abstract] [Full Text] [PDF]

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