CV effects of vasopressin

Vasopressin acts directly via V1a receptors to cause vasoconstriction. This occurs most strongly in peripheral arterioles as well as in the vasculature of the heart, brain, and kidneys. The V1a receptor (specifically, the arginine vasopressin receptor 1A or AVPR1A) is a G-protein coupled receptor that exerts its effects by activating phospholipase C, causing production of inositol triphosphate, and ultimately increasing the concentration of intracellular calcium.

There is no direct inotropic or chronotropic effect of vasopressin on the heart. Since it does not directly increase myocardial oxygen demand, it may be preferred to epinephrine in treating cardiac arrest, but several studies have found no such benefit. Under current ACLS guidelines, one dose of 40 units of vasopressin may replace the first or second dose of 1mg epinephrine.

Vasopressin may be used as an adjunct agent in vasodilatory shock, and can help decrease doses required of other agents (e.g. can be added to norepinephrine in septic shock to increase blood pressure and decrease norepinephrine requirements). As an indirect effect, heart rate and cardiac output may decrease in response to vasopressin induced increases in systemic vascular resistance.

Vasopressin has a rapid onset of action and a short half-life of 10-20 minutes. Rebound hypotension may occur with abrupt cessation of vasopressin and thus it should be gradually tapered off.

Vasopressin acts on V2 receptors in the kidneys to cause increased permeability to water in the renal tubule, resulting in water retention and more concentrated urine.