Vasopressin (AVP), the antidiuretic hormone, is a cyclic nonapeptide involved in the homeostasis of body fluid, blood volume, vascular tone, and blood pressure. AVP also belongs to the family of vasoactive and mitogenic peptides involved in physiological and pathological cell growth and differentiation¹.

AVP exerts its actions through binding to specific V_1A, V_1B, and V₂, membrane receptors coupled to distinct second messengers². V₁ AVP receptor has the typical features of a G-protein coupled transmembrane receptor with seven putative hydrophobic domains, connected by three extracellular and three intracellular loops³.

V₁ receptors activate phospholipases A2, C, and D, resulting in the production of inositol 1,4,5-trisphosphate (IPS) and 1,Z-diacylglycerol (DAG), the mobilization of intracellular Ca²⁺, the influx of extracellular Ca²⁺, the activation of protein kinase C, and protein phosphorylation⁴. V_1A AVP receptors have been shown by radioligand binding techniques to be present in vascular smooth muscle cells, hepatocytes, blood platelets, lymphocytes and monocytes, type 2 pneumocytes, adrenal cortex, brain (hippocampus septum et amygdalae), reproductive organs, retinal epithelium, renal mesangial cells, and the A10, A7r5,3T3, and WRK-1 cell lines⁴. V_1A AVP receptors mediate cell contraction and proliferation, platelet aggregation, coagulation factor release, and glycogenolysis. V_1B AVP receptors are located in the anterior pituitary where they stimulate ACTH release¹.