The vasoconstrictor endothelin-1 (ET-1) has been implicated in the pathogenesis of cerebral vasospasm and delayed cerebral ischemia following subarachnoid hemorrhage.

Endothelin-1 (ET-1) seems to represent the contractile component in a network to modulate arterial tone, with NO representing the relaxant component.

ET-1 is synthesized by vascular endothelial or smooth muscle cells. Endothelin Converting Enzyme-1 (ECE-1) is localized predominantly to endothelial cells, the apparent primary source of ET-1.

The synthesis of ET-1 seems to be enhanced in the central nervous system in pathological conditions. Increased levels of ET-1 have been found in cerebrospinal fluid (CSF)and brain tissue after trauma, ischemia, and SAH.