role of vasopressin (ADH) in development of hyponatraemia

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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


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

Last reviewed 08/2021