In addition, SAH can cause endothelial dysfunction immediately, and adverse factors, such as neuroinflammation and oxidative stress, promote the release of a large number of vasoconstrictors, such as ET-1, NPY [22, 30], and, especially IL-1β, which can induce the synthesis of additional ET-1, the strongest vasoconstrictor currently known. This evidence concerns the gene IL1B and endothelial dysfunction.