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.
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