Vasopressin is the exogenous, parenteral form of antidiuretic hormone (ADH) that may be used for several conditions in the intensive care unit (ICU), including the treatment of central diabetes insipidus and as a vasopressor agent in shock. Endogenous vasopressin is an important stress hormone and plays a critical role in maintaining volume hemostasis. However, its beneficial physiological effects may be offset when there is excess hormone in the circulation. It is important to understand vasopressin’s mechanism of action and to be able to recognize which ICU patients may suffer adverse effects from the use of this drug.

Endogenous vasopressin is synthesized in neurosecretory cells of the hypothalamus and excreted by the posterior pituitary gland in response to decreases in blood volume and increases in serum osmolality. Receptors for vasopressin are primarily located in vascular smooth muscle (V₁) and the renal collecting duct (V₂) and act to stimulate vasoconstriction and increase free water reabsorption, respectively. These are normal compensatory mechanisms designed to maintain vascular tone and circulatory homeostasis during periods of low cardiac output.