Register for email alerts and news feeds:
This journal | BMJ Group
rss
Heart 2005;91:1275-1277; doi:10.1136/hrt.2005.061325
Copyright © 2005 BMJ Publishing Group Ltd & British Cardiovascular Society

MINI-SYMPOSIUM

Genetic regulation of endothelial function

L C Jones, A D Hingorani

Centre for Clinical Pharmacology, British Heart Foundation Laboratories, Department of Medicine, University College London, London, UK

Correspondence to:
Correspondence to:
Dr Aroon D Hingorani
Centre for Clinical Pharmacology, BHF Laboratories, Department of Medicine, 5 University Street, London WC1E 6JJ, UK; a.hingorani@ucl.ac.uk

Abbreviations: ADMA, asymmetric dimethylarginine; BH4, tetrahydrobiopterin; DDAH, dimethylarginine dimethylaminohydrolases; EDHF, endothelium derived hyperpolarising factor; eNOS, endothelial nitric oxide synthase; FMD, flow mediated dilatation; LDL, low density lipoprotein; NO, nitric oxide; O2, superoxide; ROS, reactive oxygen species

Keywords: endothelial function; genetic regulation; nitric oxide

The first 150 words of the full text of this article appear below.

The healthy vascular endothelium exerts atheroprotective actions through vasoactive mediators such as nitric oxide (NO), prostacyclin, and endothelium derived hyperpolarising factor (EDHF). There is evidence that as the endothelium ages, it is exposed to the damaging effects of raised blood pressure and increased concentrations of cholesterol, glucose, homocysteine, to products of the inflammatory response, and to the constituents of cigarette smoke, and these protective properties diminish leading to a state of endothelial dysfunction.1 Endothelial dysfunction can be detected in forearm or coronary arteries in vivo, before the development of clinical atherosclerosis, as an impairment of endothelium dependent agonist or flow mediated vasodilation.2 Endothelial dysfunction by these methods correlates with cardiovascular risk factors,3 and may be predictive of incident cardiovascular events.4

Children with certain single gene disorders such as homocystinuria and familial hypercholesterolaemia, at risk of premature atherosclerosis, also exhibit early endothelial dysfunction.5,6 Although the more common forms of atherosclerosis manifest . . . [Full text of this article]


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?

This article has been cited by other articles:

  • Barac, A., Campia, U., Panza, J. A. (2007). Methods for Evaluating Endothelial Function in Humans. Hypertension 49: 748-760 [Full Text]  

This Article

Services
Citing Articles
Google Scholar
PubMed
Topic Collections
Bookmark with

Register for free content

The full back archive is now available for all BMJ Journals. Institutional subscribers may access the entire archive as part of their subscription. Personal subscribers will also have access to all content when logged in. Non-subscribers who register have free access to all articles published before 2006 right back to volume 1 issue 1. Register here to access the free archive of all BMJ Journals.

Don't forget to sign up for content alerts so you keep up to date with all the articles as they are published.