Endothelial cell injury and the loss of cytoprotective mechanisms that involve nitric oxide, prostacyclin and endothelium-dependent hyperpolarization (EDH) are thought to underlie atherosclerosis, although how these mechanisms are anti-atherogenic is unclear. This is particularly so because thrombus formation, one of the major initiators of the disease, usually occurs at discrete luminal sites; thus, only small numbers of endothelial cells can be recruited to initiate anti-inflammatory responses. However, we, and others, have demonstrated that locally generated EDH spreads to endothelial cells and smooth muscle cells throughout a vessel to cause remote vasodilatation. In this article, we propose that, in addition to a widespread inhibitory signalling mechanism, EDH produced by the endothelium also initiates remote anti-inflammatory actions that prevent large blood vessels developing atherosclerosis.
|Pages (from-to)||213 - 220|
|Number of pages||8|
|Journal||Trends in Pharmacological Sciences|
|Publication status||Published - 2002|