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Hyponatremia Associated with Heart Failure: Pathological Role of Vasopressin-Dependent Impaired Water Excretion

Department of Medicine, Saitama Medical Center, Jichi Medical University, 1-847 Amanuma Omiya, Saitama 330-8503, Japan
Academic Editor: Lewis S. Blevins
J. Clin. Med. 2015, 4(5), 933-947; https://doi.org/10.3390/jcm4050933
Received: 8 August 2014 / Revised: 19 February 2015 / Accepted: 7 April 2015 / Published: 8 May 2015
(This article belongs to the Special Issue Hyponatremia: Advances in Diagnosis and Management)
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. View Full-Text
Keywords: hyponatremia; arginine vasopressin (AVP); aquaporin2 (AQP2); non-osmotic release; heart failure; cardiac output; circulatory blood volume; impaired water excretion; AVP V2 receptor antagonist hyponatremia; arginine vasopressin (AVP); aquaporin2 (AQP2); non-osmotic release; heart failure; cardiac output; circulatory blood volume; impaired water excretion; AVP V2 receptor antagonist
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Ishikawa, S.-E. Hyponatremia Associated with Heart Failure: Pathological Role of Vasopressin-Dependent Impaired Water Excretion. J. Clin. Med. 2015, 4, 933-947.

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