Arginine-vasopressin (AVP) is a peptide hormone classically known to be synthesized in the hypothalamus and secreted by the posterior pituitary gland. AVP has a variety of roles in the body and a variety of systemic physiologic functions to include vasoconstriction, gluconeogenesis, corticosteroidogenesis, and excretion of water and urea. AVP causes a peripheral vasoconstriction that is thought to be mediated primarily by the V1 receptor. AVP is thought to do this by a variety of mechanisms to include activation of the V1a receptors with stimulation of phospholipase A2 which leads to increased calcium spiking activity. AVP could also do this by regulating the expression of other hypertensive factors and proteins in the body. AVP has been shown to play an important role in the development of hypertension following aortic constriction in rats. When rats were given AVP following constriction of the abdominal aorta, hypertension developed and these animals had an increased response to angiotensin II. Therefore AVP is thought to permit the expression of other factors such as angiotensin II. The presence of AVP is important in other animal models of hypertension such the spontaneously hypertensive rat and DOCA salt hypertension. For instance, administration of DOCA salt to Brattleboro rats, genetically incapable of synthesizing vasopressin in the hypothalamus, will not result in the development of hypertension. However, with administration of exogenous AVP, these rats will develop hypertension when given DOCA salt treatment.