PubMed · 4080951
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P A Bacon. 1985. Evolving concepts in vasculitis.. https://pubmed.ncbi.nlm.nih.gov/4080951/
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The role of endothelium in vasodilatation has only emerged in the last ten years. It was observed that many endogenous substances from endothelial cells triggered the release of a substance which was named endothelium-derived relaxing factor (EDRF). Later has been showed that NO accounted for most if not all of the biological activity of EDRF. The endothelial synthesis of NO originates from L-arginine and could be blocked by the methyl analogue (e.g. NG-mono-methyl-L-arginine). Beside endothelial cells NO could be identified in several mammalian tissues including brain, hepatocytes, lung and macrophages. NO mediated the control of vascular tone and blood pressure via vascular smooth muscle cells which exert relaxation and constriction of blood vessels. It is considered NO represents signal for the guanylate cyclase system which regulates the intracellular concentration of Ca2+ ions. It is well known that the concentration of Ca2+ ions play discern direct role in the relaxation and contraction of smooth muscle, respectively.
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Current literature on the pathogenesis of the hemolytic-uremic syndrome (HUS) is analyzed. A variety of etiologic factors and mechanisms of HUS development is considered. The emphasis is laid on the endotoxinemia, damage of the renal vessel and glomerular mesangium endothelium and other mechanisms.