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Cardiovascular Research 2004 63(1):1-4; doi:10.1016/j.cardiores.2004.04.028
© 2004 by European Society of Cardiology
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Copyright © 2004, European Society of Cardiology

The multi-faceted behavior of nitric oxide in vascular "inflammation": catchy terminology or true phenomenon?

Isabella Tritto and Giuseppe Ambrosio*

Division of Cardiology, University of Perugia School of Medicine, Ospedale Silvestrini, via S. Andrea delle Fratte, 06156 Perugia, Italy

*Corresponding author. Tel.: +39-75-527-1509; fax: +39-75-527-1244. Email address: giuseppe.ambrosio@ospedale.perugia.it

Received 19 April 2004; accepted 23 April 2004

Abbreviations: NO, nitric oxide • OFRs, oxygen free radicals • ONOO•, peroxynitrite • VSMCs, vascular smooth muscle cells • •O2–, superoxide radical

The first 10% of the full text of this article appears below.

See article by Hattori et al. [11] (pages 31–40) in this issue.

Over the last 20 years, our understanding of the role of nitric oxide (NO) in biological systems has evolved enormously. Once considered merely a vasodilator (albeit a very powerful one), NO has subsequently attracted attention for its ability to modulate a number of intracellular pathways at the vascular and extravascular level. This is, however, when the headache began. The flurry of studies investigating a variety of possible cellular targets soon led to the discovery that, under different conditions, several pathophysiological events could be affected by NO by seemingly divergent mechanisms.

Initial studies pointed towards a protective effect of NO on cellular activities, indicating that NO would prevent development of the pro-atherogenic phenotype in endothelial cells and vascular smooth muscle cells, reduce leukocyte adhesion and recruitment . . . [Full Text of this Article]


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