Skip Navigation

Cardiovascular Research 2008 77(1):19-29; doi:10.1016/j.cardiores.2007.06.024
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (1)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Liu, V. W.T.
Right arrow Articles by Huang, P. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Liu, V. W.T.
Right arrow Articles by Huang, P. L.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© European Society of Cardiology 2007. All rights reserved.For permissions please email: journals.permissions@oxfordjournals.org

Cardiovascular roles of nitric oxide: A review of insights from nitric oxide synthase gene disrupted mice{dagger}

Victor W.T. Liu and Paul L. Huang*

Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School, Boston,MA 02114, United States

* Corresponding author. Cardiovascular Research Center, Massachusetts General Hospital East, 149 Thirteenth Street, Charlestown, MA 02129. Tel: +1 617 724 9849; fax: +1 617 726 5806. E-mail address: phuang1{at}partners.org (P.L. Huang).

Nitric oxide (NO) is a gaseous molecule that plays many key roles in the cardiovascular system. Each of the enzymes that generate NO—neuronal, inducible and endothelial NO synthase—has been genetically disrupted in mice. This review discusses the cardiovascular phenotypes of each of the NO synthase (NOS) gene knockout mice, and the insights gained into the roles of NO in the cardiovascular system. Mice lacking the endothelial isoform are hypertensive, have endothelial dysfunction and show a more severe outcome in response to vascular injury, to stroke and cerebral ischaemia, and to diet-induced atherosclerosis. Mice lacking the neuronal isoform show a less severe outcome in response to stroke and cerebral ischaemia but have increased diet-induced atherosclerosis. Mice lacking the inducible isoform show reduced hypotension to septic shock. Together, NOS gene knockout mice have been useful tools that complement our other approaches to studying the multiple roles of NO in the cardiovascular system.

KEYWORDS Nitric oxide; Gene knockout; Targeted disruption; Animal models; Pathophysiology; Atherosclerosis; Vascular dysfunction; Cerebral ischaemia; Mouse models

Time for primary review: 20 days

{dagger} This article was published online by Elsevier on 30 June, 2007.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Circ Cardiovasc GenetHome page
D. R. Fermin, A. Barac, S. Lee, S. P. Polster, S. Hannenhalli, T. L. Bergemann, S. Grindle, D. B. Dyke, F. Pagani, L. W. Miller, et al.
Sex and Age Dimorphism of Myocardial Gene Expression in Nonischemic Human Heart Failure
Circ Cardiovasc Genet, December 1, 2008; 1(2): 117 - 125.
[Abstract] [Full Text] [PDF]

Home page
 Arterioscler. Thromb. Vasc. Bio.Home page
F. Kim, M. Pham, E. Maloney, N. O. Rizzo, G. J. Morton, B. E. Wisse, E. A. Kirk, A. Chait, and M. W. Schwartz
Vascular Inflammation, Insulin Resistance, and Reduced Nitric Oxide Production Precede the Onset of Peripheral Insulin Resistance
Arterioscler Thromb Vasc Biol, November 1, 2008; 28(11): 1982 - 1988.
[Abstract] [Full Text] [PDF]

Home page
 Circ. Res.Home page
C. C. Matouk and P. A. Marsden
Epigenetic Regulation of Vascular Endothelial Gene Expression
Circ. Res., April 25, 2008; 102(8): 873 - 887.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.