Vasopressin release, water channels, and vasopressin antagonism in cardiac failure, cirrhosis, and pregnancy

Schrier, R. W., Fassett, R. G., Ohara, M. and Martin, P. Y. (1998) Vasopressin release, water channels, and vasopressin antagonism in cardiac failure, cirrhosis, and pregnancy. Proceedings of the Association of American Physicians, 110 5: 407-411.

Author Schrier, R. W.
Fassett, R. G.
Ohara, M.
Martin, P. Y.
Title Vasopressin release, water channels, and vasopressin antagonism in cardiac failure, cirrhosis, and pregnancy
Journal name Proceedings of the Association of American Physicians   Check publisher's open access policy
ISSN 1081-650X
Publication date 1998-09
Sub-type Article (original research)
Volume 110
Issue 5
Start page 407
End page 411
Total pages 5
Publisher Elsevier
Language eng
Abstract Vasopressin (AVP) is released in response to both osmotic and nonosmotic stimuli. Nonosmotic-stimulated AVP release occurs in cardiac failure, cirrhosis, and pregnancy in response to alterations in arterial circulatory integrity. Cardiac failure in rats is associated with increased plasma AVP and hypothalamic AVP mRNA, and in humans, it is associated with cardiac failure. Plasma AVP concentrations are elevated when measured with a sensitive radioimmunoassay. Urinary concentrations of AVP-responsive aquaporin-2 water channels are also elevated in cardiac failure. V2 receptor antagonists correct the impaired solute-free water excretion seen in rats with low-output cardiac failure and reverse the upregulation of renal aquaporin-2 water channels. Orally active non-peptide-selective V2 receptor antagonists administered to patients with congestive cardiac failure decrease urinary concentrations of aquaporin-2, increase solute-free water clearance, and correct the hyponatremia. Cirrhosis of the liver results in splanchnic arterial vasodilation and increased vascular capacity, most likely secondary to increased nitric oxide production. This relative underfilling of the arterial circulation stimulates nonosmotic AVP release with resultant water retention. Aquaporin-2 gene expression is upregulated in the kidneys of rats with cirrhosis of the liver. AVP-2 receptor antagonists administered to animals with cirrhosis reverse the water retention. Human studies using orally active, non-peptide-selective V2 receptor antagonists in patients with cirrhosis are currently underway. Pregnancy is another state of nitric oxide- mediated arterial vasodilation that is associated with plasma AVP concentrations that are relatively high for the degree of hypoosmolality. Upregulation of the water channel aquaporin-2 in the renal papillae of pregnant rats has also been demonstrated, and this effect is reversed by administration of a V2 receptor antagonist.
Keyword Hyponatremia
Edematous disorders
Arterial underfilling
Nitric oxide
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Unknown

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Medicine Publications
Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 26 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 0 times in Scopus Article
Google Scholar Search Google Scholar
Created: Wed, 09 Mar 2011, 08:46:28 EST