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(Hypertension. 2007;50:e156.)
© 2007 American Heart Association, Inc.

Letters to the Editor

Aldosterone Rapidly Induces Leukocyte Adhesion to Endothelial Cells: A New Link Between Aldosterone and Arteriosclerosis?

Carl Gustav Carus University Hospital, Medical Clinic III, University of Dresden, Dresden, Germany

Michael Gekle

Julius-Bernstein-Institut für Physiologie, University Halle-Wittenberg, Halle, Germany

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

To the Editor:

Aldosterone is known to induce cardiovascular dysfunction, including fibrosis, inflammation, and endothelial dysfunction, as well as thrombosis formation.¹ Clinical trials have shown aldosterone to be an independent predictor of increased mortality in patients with chronic heart failure,² and high circulating plasma aldosterone levels predict the clinical outcome in patients after myocardial infarction.³ Mineralocorticoid receptor blockade proved to exert beneficial effects in clinical trials, such as the Randomised Aldactone Evaluation Study and the Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study.⁴ Recent studies provided evidence for a role of aldosterone in the pathogenesis of arteriosclerosis.⁵ However, the exact mechanisms of adverse aldosterone actions in the cardiovascular system are largely unknown. Here, we aimed at elucidating rapid (60 minutes) aldosterone effects on interactions between endothelial cells and leukocytes.

We performed adhesion experiments using primary cultures of freshly isolated human endothelial cells from the umbilical cord vein (HUVECs) and polymorphonuclear leukocytes (PMNs).⁶ Adhesion of leukocytes is mediated by adhesion molecules such as intercellular adhesion molecule-1, vascular cell adhesion molecule-1 and e-selectin.⁷ Therefore, we assessed expression of these molecules by Western blot analysis and immunohistochemistry⁸ in isolated HUVECs and human umbilical artery endothelial cells.

Figure 1A shows stimulated adhesion of PMNs to a monolayer of HUVECs after incubation of endothelial cells with increasing aldosterone concentrations (1 to 100 nmol/L). The effect observed was concentration dependent, indicating specificity for aldosterone. Leukocyte adhesion reaches a maximum after 1 hour with no further increase (Figure 1B). Figure 1C . . . [Full Text of this Article]

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