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(Hypertension. 2005;45:185.)
© 2005 American Heart Association, Inc.

Editorial Commentaries

Beyond Blood Pressure

Endothelial Protection Against Hypercholesterolemia by Angiotensin II Type-1 Receptor Blockade

From the Department of Vascular Endothelium and Microcirculation, Medical Faculty Carl Gustav Carus, University of Technology Dresden, Germany.

Correspondence to Henning Morawietz, PhD, Department of Vascular Endothelium and Microcirculation, Medical Faculty Carl Gustav Carus, University of Technology Dresden Fetscherstr. 74 D-01307 Dresden, Germany. E-mail Henning.Morawietz@mailbox.tu-dresden.de

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

Hypercholesterolemia and an activated renin-angiotensin-aldosterone system are well-established independent cardiovascular risk factors. Several lines of evidence support an important role of modified LDLs and angiotensin II in the development and progression of atherosclerosis. Angiotensin II is not only a potent vasoconstrictor, but it also promotes proinflammatory and prothrombotic properties of vascular cells. A growing body of in vitro studies shows the induction of cellular adhesion molecules and cytokines by angiotensin II in endothelial cells.¹ In vivo, angiotensin II promotes leukocyte–endothelial cell interaction in the microcirculation. This proinflammatory mechanism involves the redox-sensitive mobilization of adhesion molecules such as P-selectin.^2,3 These and several additional findings in cell systems and large vessels support a crucial role of the angiotensin II type-1 (AT₁) receptor–mediated formation of reactive oxygen species (ROS) in the pathogenesis of atherosclerosis.^4,5 However, the impact of AT₁ receptor antagonism on the accelerated inflammatory and thrombotic response and ROS formation by hypercholesterolemia has not been studied in the microvasculature in vivo so far.

In this issue of Hypertension, Petnehazy et al provide experimental evidence for the endothelial protection by AT₁ receptor antagonism against inflammatory and thrombogenic responses to hypercholesterolemia.⁶ The authors describe in this very interesting study a decreased platelet and leukocyte adhesion after losartan treatment in postcapillary venules of mice with hypercholesterolemia. This endothelial protection is not mediated by direct effects on blood pressure or serum cholesterol. The systemic AT₁ receptor antagonism prevents the augmented oxidative stress in hypercholesterolemic microcirculation. Hypercholesterolemia increases AT₁ receptor expression itself, which is prevented . . . [Full Text of this Article]

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				H. Morawietz, S. Erbs, J. Holtz, A. Schubert, M. Krekler, W. Goettsch, O. Kuss, V. Adams, K. Lenk, F. W. Mohr, et al. Endothelial Protection, AT1 Blockade and Cholesterol-Dependent Oxidative Stress: The EPAS Trial Circulation, July 4, 2006; 114(1_suppl): I-296 - I-301. [Abstract] [Full Text] [PDF]