Endothelium-dependent hyperpolarization as a remote anti-atherogenic mechanism

Stavros Selemidis, Thomas M Cocks

Research output: Contribution to journalArticleResearchpeer-review

18 Citations (Scopus)

Abstract

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.
Original languageEnglish
Pages (from-to)213 - 220
Number of pages8
JournalTrends in Pharmacological Sciences
Volume23
Issue number5
Publication statusPublished - 2002

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