Synthesis, release, and action of vasopressin
Vasopressin is a 9-amino-acid peptide that is synthesized in the nerve bodies in the supraoptic and paraventricular nuclei of the hypothalamus and is secreted from the posterior pituitary gland.1
Secretion of vasopressin is normally stimulated by increased plasma osmolality via activation of osmoreceptors in the anterior hypothalamus and by decreased blood volume or pressure via activation of baroreceptors in the carotid sinus, aortic arch, cardiac atria, and pulmonary venous system.1,2
The primary role of vasopressin, or antidiuretic hormone, is to control the body's water, electrolyte balance, and blood pressure, by influencing the water excretion by the kidney. Vasopressin contributes to homeostasis by promoting the reabsorption of fluid through the V2-receptors by binding to these receptors, causing the translocation of aquaporin-2 water channels to the apical membrane in the collecting duct of the kidney.2,3
Adapted from Finley, Circulation, 2008.
Vasopressin V2-receptor activation: The binding of vasopressin to the V2-receptor stimulates a Gs-coupled protein that activates adenylyl cyclase, in turn causing production of cAMP to activate protein kinase A. This pathway increases the exocytosis of aquaporin water
channel–containing vesicles and inhibits endocytosis of the vesicles, both resulting in increases in aquaporin-2 channel formation and apical membrane insertion. This allows an increase in the permeability of water from the collecting duct.4
Relationship of vasopressin to hyponatremia
Inappropriately elevated plasma levels of vasopressin increase water reabsorption and retention, which will disproportionately expand the plasma volume, thus resulting in dilutional hyponatremia.2
In patients with syndrome of inappropriate antidiuretic hormone (SIADH), vasopressin release is not fully suppressed, despite hypo-osmolality, owing to other causes, including ectopic production of vasopressin by some tumors. The persistence of vasopressin release due to nonosmotic hemodynamic stimuli is also predominantly responsible for water retention and hyponatremia with hypervolemia and edema-forming disorders, such as heart failure.2
Adapted from Knoers, N Engl J Med, 2005.
V2-receptors control the antidiuretic effect of vasopressin from their position in the renal collecting tubules. Antagonizing these receptors can produce solute-sparing water excretion.2