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Arginine vasopressin (AVP), also known as antidiuretic hormone (ADH), is a peptide hormone synthesized in the hypothalamus and subsequently released by the posterior pituitary gland in response to increased plasma osmolality or decreased blood volume. AVP primarily acts as an antidiuretic by binding to V2 receptors in the kidney, increasing water reabsorption and thus concentrating urine. It also mediates vasoconstriction through V1A receptors, contributing to regulation of blood pressure. AVP is synthesized as part of a larger precursor peptide (preprovasopressin), which is processed to yield AVP, neurophysin II (carrier protein), and copeptin (a biomarker). Dysfunction of AVP production or its action results in disorders such as central or nephrogenic diabetes insipidus and contributes to conditions like hyponatremia and shock. AVP analogues (such as desmopressin) and antagonists are important therapeutic agents in the management of these disorders.
Agonism at V2 receptor increases water reabsorption at kidney collecting ducts via cAMP/Aquaporin-2 pathway (e.g., Desmopressin, AVP). Antagonism at V2 receptor promotes free water excretion (e.g., Tolvaptan). Agonism at V1A receptor leads to vasoconstriction and blood pressure support (high AVP doses, some shock therapies). Antagonism at V1A receptor causes blockade of vasoconstrictor effects. Agonism/antagonism at V1B/V3 receptor modulates pituitary ACTH release and the stress response.
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