Rheumatology 2002; 41: 843-847
© 2002 British Society for Rheumatology
Editorial |
Beauty and the Beast. The nitric oxide paradox in systemic sclerosis
Department of Medicine, Division of Rheumatology, University of Florence, Italy and
1 Department of Medicine, Division of Rheumatology, Medical College of Ohio, Toledo, OH, USA
| The first 150 words of the full text of this article appear below. |
Vascular endothelial dysfunction is a central event in the pathogenesis of a variety of human diseases, including systemic sepsis, ischaemia–reperfusion injury, adult respiratory distress syndrome, atherosclerosis and diffuse systemic inflammatory disorders.
In systemic sclerosis (SSc), the microvascular bed is the target of an immune–inflammatory injury that leads to dysregulation of vascular tone control and results in progressive disorganization of the vascular architecture, leading to vascular obliteration and diminished blood flow to the organs involved [1]. On the cellular level, endothelial dysfunction is characterized by a shift in the endothelial functional profile towards an inflammatory and vasospastic functional potential [2]. Raynaud's phenomenon (RP) is the most recognizable clinical sign that reflects this dysfunction. Several pathological mechanisms have been proposed as potential causes of RP [3]. The endothelial hypothesis suggests reduced production of the endothelium-derived vasodilatory mediators [prostacyclin, nitric oxide (NO)] and increased endothelial vasoconstrictive signals
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