Abstract
An exaggerated increase in circulatory blood volume is linked to congestive heart failure. Despite this increase, reduction of the “effective circulatory blood volume” in congestive heart failure is associated with decreased cardiac output, and can weaken the sensitivity of baroreceptors. Thereafter, tonic inhibition of the baroreceptor-mediated afferent pathway of vagal nerves is removed, providing an increase in non-osmotic release of arginine vasopressin (AVP). In the renal collecting duct, the aquaporin-2 (AQP2) water channel is regulated by sustained elevation of AVP release, and this leads to augmented hydroosmotic action of AVP, that results in exaggerated water retention and dilutional hyponatremia. Hyponatremia is also a predictor for worsening heart failure in patients with known/new onset heart failure. Therefore, such a dilutional hyponatremia associated with organ damage is predictive of the short- and long-term outcome of heart failure.
Highlights
An exaggerated increase in circulatory plasma volume is linked to organ disorders such as congestive heart failure, decompensated liver cirrhosis and nephrotic syndrome, in which non-osmotic release of arginine vasopressin (AVP) is associated with an increase in water permeability in cells of
The present review paper demonstrated hyponatremia is associated with heart failure
Impaired renal water excretion is closely associated with an exaggerated release of AVP in heart failure
Summary
An exaggerated increase in circulatory plasma volume is linked to organ disorders such as congestive heart failure, decompensated liver cirrhosis and nephrotic syndrome, in which non-osmotic release of arginine vasopressin (AVP) is associated with an increase in water permeability in cells of. Sustained AVP-dependent antidiuresis produces water retention, increasing the circulatory blood volume in congestive heart failure. An excessive circulatory plasma volume results in dilutional (hypervolemic) hyponatremia [3]. The pathogenesis of impaired water excretion in congestive heart failure is examined in this review. The physiological control of AVP release, and inappropriate release of AVP in heart failure are described. The augmented hydroosmotic action of AVP and expression of aquaporin-2 (AQP2) water channel are discussed in association with water retention. The ability of organ damage-related dilutional hyponatremia to predict long-term outcome in heart failure is examined
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