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Arteriosclerosis, Thrombosis, and Vascular Biology. 2003;23:1218-1223
Published online before print May 22, 2003, doi: 10.1161/01.ATV.0000078521.51319.65
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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2003;23:1218.)
© 2003 American Heart Association, Inc.

Vascular Biology

Angiotensin II Inhibits Endothelial Cell Motility Through an AT1-Dependent Oxidant-Sensitive Decrement of Nitric Oxide Availability

Giovambattista Desideri; Maria Cristina Bravi; Marzia Tucci; Giuseppe Croce; Maria Contina Marinucci; Anna Santucci; Edoardo Alesse; Claudio Ferri

From Department of Internal Medicine and Public Health and Department of Experimental Medicine (E.A.), University of L’Aquila, Italy.

Correspondence to Giovambattista Desideri, MD, University of L’Aquila, Department of Internal Medicine and Public Health, Via Vetoio, Blocco 11, 67100, Coppito, L’Aquila, Italy. E-mail giovambattista.desideri{at}cc.univaq.it

Objective— The migratory capability of vascular endothelial cells plays a pivotal role in the maintenance of vessel wall integrity and is stimulated by nitric oxide (NO). Angiotensin II increases NAD(P)H oxidase activity in endothelial cells, thereby promoting reactive oxygen species (ROS) generation. Because ROS can both reduce NO synthase activity and increase NO breakdown, thus impairing NO availability in endothelial cells, we evaluated the effect of angiotensin II on human vascular endothelial cell (HUVEC) motility.

Methods and Results— Angiotensin II dose- and time-dependently reduced HUVEC migration. Besides inhibiting HUVEC motility, angiotensin II altered intracellular glutathione redox status. The generation of ROS by cultured HUVECs was significantly increased by angiotensin II. Furthermore, angiotensin II reduced NO metabolite concentrations in culture media. The angiotensin II type 1 receptor antagonist candesartan cilexetil attenuated the inhibitory action exerted by angiotensin II on HUVEC motility, reversed the angiotensin II-induced increase in intracellular oxidative stress, and restored NO availability. Similar effects were exerted by the flavonoid inhibitor diphenylene iodinium and the antioxidant agent N-acetyl-L-cysteine.

Conclusions— All together, our data demonstrate that angiotensin II inhibits HUVEC motility by reducing NO availability. Such reduction is due to an angiotensin II type 1 receptor-dependent increment in intracellular ROS generation.


Key Words: angiotensin II • endothelium • migration • oxidative stress • glutathione




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