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 non-osmotic 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
- AVP secretion is normally stimulated by
Reference:
- Adrogué HJ, Tucker BM, Madias NE. Diagnosis and management of hyponatremia: a review. JAMA. 2022 Jul 19;328(3):280-91.
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