Endothelial alterations in hypercholesterolemia: More than simply vasodilator dysfunction Article Conference Paper uri icon

Overview

MeSH Major

  • Vascular Diseases

abstract

  • Occlusive vascular disease begins with an alteration of the endothelium, which is characterized by a decrease in nitric oxide (NO) activity. Endogenous NO inhibits many key processes in atherogenesis, including monocyte adherence, platelet activation, and smooth muscle proliferation. The mechanism by which NO activity is reduced in hypercholesterolemia and in other metabolic disorders associated with atherogenesis appears to be multifactorial. It includes increased production of oxygen-derived free radicals, alterations in NO synthase, and the accumulation of endogenous inhibitors (ADMA) of NO synthase. Plasma concentrations of ADMA are elevated in hypercholesterolemic humans. Elevated ADMA concentrations are associated with impaired endothelium-dependent, NO-mediated vasodilatation and reduced urinary nitrate exertion. These effects of ADMA are counteracted by administration of the NO precursor L-arginine. It is likely that basic insights regarding the mechanisms of endothelial dysfunction will lead to new therapeutic strategies for atherosclerosis.

publication date

  • December 1998

Research

keywords

  • Conference Paper

Identity

PubMed ID

  • 9883748

Additional Document Info

start page

  • S48

end page

  • 53

volume

  • 32

number

  • SUPPL. 3