MINI-SYMPOSIUM
Genetic regulation of endothelial function
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
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Barac, A., Campia, U., Panza, J. A.
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