These findings suggest a series of events where 1) the drop in blood flow and wall tension experienced by the cerebral arteries during SAH triggers early activation of the MEK-ERK1/2 pathway, which 2) triggers increased expression and contractile function of vasoconstrictor receptors in cerebral arteries during the following days, where 3) the resulting enhanced cerebrovascular contractility contribute to development of delayed cerebral ischemia evident as CBF reduction, neurological deficits and mortality. This evidence concerns the gene MAP2K7 and brain ischemia.