The calcium antagonistic effects of magnesium can also affect the cerebral endothelium that forms the blood-brain barrier. Decreased cell calcium inhibits endothelial contraction and opening of tight junctions that are linked to the actin cytoskeleton. Decreased tight junction permeability limits paracellular transport of vascular contents, ions and proteins, which can promote vasogenic edema and seizures. It is also possible that magnesium sulfate diminishes transcellular transport by limiting pinocytosis that is known to occur rapidly during acute hypertension. Magnesium may also downregulate aquaporin 4 (AQP4), a water channel protein localized to astrocytic endfeet, and possibly cerebral endothelium, that is associated with cerebral edema formation (through unknown mechanisms).