What is the mode of action of Vasopressin?

From the Guidelines

Vasopressin works by reducing blood flow to splanchnic organs, thereby decreasing portal venous inflow and portal pressure through its potent vasoconstrictive properties.

Mode of Action

• Vasopressin is a potent splanchnic vasoconstrictor, which reduces blood flow to all splanchnic organs, leading to a decrease in portal venous inflow and portal pressure 1.
• Its clinical usefulness is limited by its multiple side effects, which are related to its potent vasoconstrictive properties, including cardiac and peripheral ischemia, arrhythmias, hypertension, and bowel ischemia 1.
• The addition of nitrates, such as nitroglycerin, can improve the efficacy and safety of vasopressin, but side effects of combination therapy are still higher than those associated with terlipressin, somatostatin, or somatostatin analogues 1.

Dosage and Administration

• Vasopressin is administered at a continuous IV infusion of 0.2-0.4 units/minute, which can be increased to a maximal dose of 0.8 units/minute 1.
• It should always be accompanied by IV nitroglycerin at a starting dose of 40 µg/minute, which can be increased to a maximum of 400 µg/minute, adjusted to maintain a systolic blood pressure of 90 mmHg 1.
• The duration of treatment with vasopressin is limited to 24 hours to minimize the development of side effects 1.

From the Research

Mode of Action of Vasopressin

The mode of action of vasopressin involves several key mechanisms:

• Vasopressin, also known as antidiuretic hormone (ADH), plays a crucial role in water maintenance in the body through its antidiuretic actions in the kidney 2.
• The effects of vasopressin include activation of V2 receptors, which stimulate the formation of cyclic AMP (cAMP) and phosphorylation of water channels aquaporin 2 (AQP2) in the collecting duct 2.
• Vasopressin also has vasoconstrictor effects through V1a receptors in the vasculature, while V1b is found in the nervous system 2, 3.
• The activation of V1a and V1b receptors increases intracellular Ca2+, while the activation of V2 receptors is related to cAMP-dependent phosphorylation in kidney collecting ducts, acting in coordination to stimulate water and electrolyte homeostasis 2.

Cellular Electrophysiological Actions

The cellular electrophysiological actions of vasopressin include:

• Enhancing membrane excitability and modulating synaptic transmission 3.
• Generating a cationic inward current and/or reducing a potassium conductance in motoneurons 3.
• Enhancing the inhibitory synaptic input to motoneurons 3.
• Exciting a subpopulation of neurons in the amygdala and lateral septum, while indirectly inhibiting other neurons 3.

Clinical Applications

Vasopressin has potential clinical applications in the treatment of various shock states, including:

• Septic shock, where it has marked vasopressor effects even at low doses 4, 5.
• Hypovolaemic shock, ventricular fibrillation, and cardiopulmonary bypass 4.
• The use of vasopressin in these conditions is thought to be due to its ability to inhibit pathologic vasodilator processes and produce greater blood flow diversion to vital organs 4, 5.