Donate Help Contact The AHA Sign In Home
American Heart Association
Arteriosclerosis, Thrombosis, and Vascular Biology
Search: search_blue_button Advanced Search
« Previous Article | Table of Contents | Next Article »
Arteriosclerosis, Thrombosis, and Vascular Biology. 2003;23:1218-1223
Published online before print May 22, 2003, doi: 10.1161/01.ATV.0000078521.51319.65
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
23/7/1218    most recent
01.ATV.0000078521.51319.65v1
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Desideri, G.
Right arrow Articles by Ferri, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Desideri, G.
Right arrow Articles by Ferri, C.
Related Collections
Right arrow Health policy and outcome research
Right arrow Cardiac development
(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




This article has been cited by other articles:


Home page
 J. Nutr.Home page
D. Grassi, A. Aggio, L. Onori, G. Croce, S. Tiberti, C. Ferri, L. Ferri, and G. Desideri
Tea, Flavonoids, and Nitric Oxide-Mediated Vascular Reactivity
J. Nutr., August 1, 2008; 138(8): 1554S - 1560S.
[Abstract] [Full Text] [PDF]

Home page
 HypertensionHome page
X. Yu, K. Murao, H. Imachi, W.-M. Cao, J. Li, K. Matsumoto, T. Nishiuchi, R. A.M. Ahmed, N. C.W. Wong, H. Kosaka, et al.
Regulation of Scavenger Receptor Class BI Gene Expression by Angiotensin II in Vascular Endothelial Cells
Hypertension, June 1, 2007; 49(6): 1378 - 1384.
[Abstract] [Full Text] [PDF]

Home page
 Cancer Res.Home page
J. Murtagh, H. Lu, and E. L. Schwartz
Taxotere-Induced Inhibition of Human Endothelial Cell Migration Is a Result of Heat Shock Protein 90 Degradation
Cancer Res., August 15, 2006; 66(16): 8192 - 8199.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
L. Moldovan, K. Mythreye, P. J. Goldschmidt-Clermont, and L. L. Satterwhite
Reactive oxygen species in vascular endothelial cell motility. Roles of NAD(P)H oxidase and Rac1
Cardiovasc Res, July 15, 2006; 71(2): 236 - 246.
[Abstract] [Full Text] [PDF]

Home page
 CirculationHome page
M. Iwai, R. Chen, Z. Li, T. Shiuchi, J. Suzuki, A. Ide, M. Tsuda, M. Okumura, L.-J. Min, M. Mogi, et al.
Deletion of Angiotensin II Type 2 Receptor Exaggerated Atherosclerosis in Apolipoprotein E-Null Mice
Circulation, September 13, 2005; 112(11): 1636 - 1643.
[Abstract] [Full Text] [PDF]

Home page
 CirculationHome page
F. Cipollone, C. Ferri, G. Desideri, L. Paloscia, G. Materazzo, M. Mascellanti, M. Fazia, A. Iezzi, C. Cuccurullo, B. Pini, et al.
Preprocedural Level of Soluble CD40L Is Predictive of Enhanced Inflammatory Response and Restenosis After Coronary Angioplasty
Circulation, December 2, 2003; 108(22): 2776 - 2782.
[Abstract] [Full Text] [PDF]


ATVB Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search
Copyright © 2003 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited.