Terlipressin is a prodrug of vasopressin. It is slowly converted in the circulation to vasopressin, providing an effective half-life of approximately 6 hours. Vasopressin causes direct vasoconstriction by stimulating vasopressin V1-receptors on vascular smooth muscle. It also has renal (antidiuretic hormone) effects via V2-receptors and central effects via V3-receptors. The density of V1-receptors in the mesenteric arterial circulation provides a basis for the relative benefit of terlipressin in the management of portal hypertension and hepatorenal syndrome. Vasoconstriction of the mesenteric circulation leads to decreased portal venous inflow and therefore reduced portal venous pressure. This can reduce bleeding from oesophageal varices; it may also reduce the sympathetic response to systemic vasodilation, which contributes to reduced renal blood flow and consequently to the hepatorenal syndrome.
Terlipressin is given by intravenous injection every 4 to 6 hours and is preferred to vasopressin, which requires continuous infusion. In hepatorenal syndrome, terlipressin is administered in conjunction with concentrated albumin . Terlipressin is less likely than vasopressin to cause ischaemic complications (intestinal, myocardial and limb ischaemia), cardiac arrhythmias and cerebrovascular events. Terlipressin, unlike vasopressin, can be administered out of intensive care and without cardiac monitoring.