Role of vasopressin (ADH) in development of hyponatraemia

Role of vasopressin in hyponatraemia

• most cases of hyponatraemia are characterized by inappropriately elevated plasma levels of arginine vasopressin (AVP)/ADH
  • AVP secretion is normally stimulated by
    • increased plasma osmolality via activation of osmoreceptors located in the anterior hypothalamus
    • decreased blood volume or pressure via activation of high- and low-pressure baroreceptors located in the carotid sinus, aortic arch, cardiac atria, and pulmonary venous system
    • AVP is secreted from the posterior pituitary and acts on the collecting duct increasing resorption of water
  • when osmolality falls below a genetically determined osmotic threshold
    • plasma AVP levels become undetectable
    • renal excretion of solute-free water (aquaresis) results to prevent decreases in plasma osmolality
    • if there is a failure to suppress AVP secretion at osmolalities below the osmotic threshold
      • this causes water retention and hyponatraemia if the intake of hypotonic fluids is sufficient
  • syndrome of inappropriate antidiuretic hormone secretion (SIADH)
    • despite hypo-osmolality AVP release is not fully suppressed
    • continued release of AVP is continued due to a variety of causes
      • including ectopic production of AVP by some tumours
  • persistence of AVP release due to nonosmotic hemodynamic stimuli is predominantly responsible for water retention and hyponatraemia with hypovolaemia
    • this persistence of AVP release also occurs in oedema forming disorders associated with hyponatraemia (hypervolaemic hyponatraemia) e.g. heart failure and cirrhosis

Reference:

• (1) hyponatraemia Treatment Guidelines 2007: Expert Panel Recommendations The American Journal of Medicine 2007; 120 (11);S1:S1-S21.