Many suggestions as to the molecular mechanisms and pathogenic factors behind CVS and delayed cerebral ischemia after SAH have been put forward, including superoxide radical generation induced by the extravasated blood [1], inflammation in the brain and the cerebral vasculature [5], reduced levels of endothelial vasorelaxant factors and elevated levels of vasoconstrictor substances, such as endothelin-1 (ET-1) and 5-hydroxytryptamine (5-HT) [6,7]. This evidence concerns the gene EDN1 and brain ischemia.