 Conivaptan, a non-selective Arginine-Vasopressin AVP V1AV2 antagonist that reduces aquaporin 4 production and promotes aquaresis, is approved for the treatment of euvolemic and hypervolemic hyponatremia. The exact cause of the observed reduction in ICP with conivaptan is uncertain. However, the mechanism most likely represents a combination of an acute pure aquaresis, removing free water from brain tissue, and a sustained down regulation of aquaporin 4 to abateslow development of CE. The V2 antagonism of conivaptan promotes free water loss, and the V1 antagonism may improve cerebral blood flow CBF and reduce blood brain barrier permeability. Notably, serum sodium tends to correlate inversely with both ICP and CE. The early use of conivaptan could potentially be used clinically to reduce CE by these means. 