[Vasopressin and blood-brain barrier]

Arginine vasopressin (AVP) has been known to exert antidiuretic action at the kidney and some neuroactive effects. In order to examine the neural effect of AVP, it is essential to clarify the mechanism of BBB transport from intraluminal side to brain. Recent basic experimental data show the most possible mechanism for the transport of peripheral AVP across the BBB is binding of V1 receptor of AVP at the capillary luminal membrane and consequently transports AVP to neuronal cell and changes in permeability of amino acid, ion and water at the BBB. An increase in peripheral AVP results in suppression of amino acid permeability and increases in transport of sodium, potassium ions and water. Our data indicate that intraventricular or venous administration of V1 receptor antagonist significantly reduces the permeabiltiy of water, electrolites and plasma from capillary to brain in experimental brain edema. V1 receptor antagonist may become new tool for the treatment of brain edema.