Artery Research

Volume 5, Issue 2, June 2011, Pages 37 - 49

Endothelial nitric oxide synthase in the vascular wall: Mechanisms regulating its expression and enzymatic function

Authors
Michael Demosthenousa, c, Charalambos Antoniadesa, c, *, Dimitris Tousoulisa, Marios Margaritisb, Kyriakoula Marinoub, Christodoulos Stefanadisa
a1st Department of Cardiology, Athens University Medical School, Ileias 8, Gerakas Attikis, 153 44 Athens, Greece
bDepartment of Experimental Physiology, Athens University Medical School, Athens, Greece
c

Authors equally contributed.

*Corresponding author. E-mail address: antoniades@vodafone.net.gr (C. Antoniades).
Corresponding Author
Charalambos Antoniades
Received 23 December 2009, Revised 26 February 2011, Accepted 24 March 2011, Available Online 21 April 2011.
DOI
10.1016/j.artres.2011.03.003How to use a DOI?
Keywords
eNOS; Nitric oxide; Tetrahydrobiopterin; Atherosclerosis
Abstract

Endothelial nitric oxide synthase (eNOS) is the main source of nitric oxide (NO) in the vascular wall, a molecule with anti-inflammatory, antithrombotic, vasorelaxant, antioxidant and finally antiatherogenic properties. eNOS is expressed in vascular endothelium, and it uses l-arginine as a substrate, while it also requires the presence of multiple co-factors such as tetrahydrobiopterin (BH4), nicotinamide adenine dinucleotide phosphate-oxidase (NADPH) and others. In the presence of BH4 deficiency, this enzyme becomes uncoupled, and it is turned into a source of superoxide radicals instead of NO. Therefore, under these conditions which are present in patients with advanced atherosclerosis, eNOS in human vascular endothelium is largely a source of reactive oxygen species, inducing in this way atherogenesis. Therefore, the aim of future therapeutic strategies targeting atherosclerosis through regulation of eNOS physiology, should take into account that up-regulation of this enzyme in the vascular wall may not lead to a respective increase of NO bioavailability and improvement of vascular homeostasis, but it may actually induce intravascular oxidative stress, if intracellular bioavailability of eNOS co-factors is not simultaneously elevated. In conclusion, eNOS plays a critical role in the regulation of vascular homeostasis, and it is a therapeutic target against atherogenesis.

Copyright
© 2011 Association for Research into Arterial Structure and Physiology. Published by Elsevier B.V. All rights reserved.
Open Access
This is an open access article distributed under the CC BY-NC license.

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Journal
Artery Research
Volume-Issue
5 - 2
Pages
37 - 49
Publication Date
2011/04/21
ISSN (Online)
1876-4401
ISSN (Print)
1872-9312
DOI
10.1016/j.artres.2011.03.003How to use a DOI?
Copyright
© 2011 Association for Research into Arterial Structure and Physiology. Published by Elsevier B.V. All rights reserved.
Open Access
This is an open access article distributed under the CC BY-NC license.

Cite this article

TY  - JOUR
AU  - Michael Demosthenous
AU  - Charalambos Antoniades
AU  - Dimitris Tousoulis
AU  - Marios Margaritis
AU  - Kyriakoula Marinou
AU  - Christodoulos Stefanadis
PY  - 2011
DA  - 2011/04/21
TI  - Endothelial nitric oxide synthase in the vascular wall: Mechanisms regulating its expression and enzymatic function
JO  - Artery Research
SP  - 37
EP  - 49
VL  - 5
IS  - 2
SN  - 1876-4401
UR  - https://doi.org/10.1016/j.artres.2011.03.003
DO  - 10.1016/j.artres.2011.03.003
ID  - Demosthenous2011
ER  -