Editorials

Improving endothelial vasomotor function

BMJ 2001; 323 doi: https://doi.org/10.1136/bmj.323.7309.352 (Published 18 August 2001) Cite this as: BMJ 2001;323:352

May reduce cardiovascular risk, but the current evidence is circumstantial

  1. Sagar N Doshi (DoshiSN@cardiff.ac.uk), British Heart Foundation research fellow,
  2. Malcolm J Lewis, professor of cardiovascular pharmacology,
  3. Jonathan Goodfellow, senior lecturer in cardiology
  1. Wales Heart Research Institute, University of Wales College of Medicine, Heath Park, Cardiff CF14 4XN

    The vascular endothelium is a confluent, cellular monolayer that lines the entire vascular compartment at the interface between blood and the vessel wall. This “organ” possesses complex endocrine and paracrine functions and is intimately concerned in controlling vasomotor tone and preventing atherosclerosis and thrombosis.1 Indeed, endothelial dysfunction plays a key part in the pathogenesis and progression of atherosclerosis.2

    An important and relatively recently discovered endothelial product is nitric oxide, a simple, highly reactive gas previously known as endothelium-derived relaxing factor. Endothelial nitric oxide itself possesses potent antiatherogenic properties, inhibits platelet aggregation, and regulates vascular tone.1 Bioavailable nitric oxide may be increased either by enhancing its production or by reducing its inactivation—for example, by reactive oxygen species, which are thought to damage the endothelium and promote atherosclerosis. Indirect measurement of bioavailable nitric oxide, through its vasodilating properties, is an extensively investigated surrogate of endothelial (vasomotor) function in clinical and experimental studies. In this …

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