© 2001 by European Society of Cardiology
Copyright © 2000, European Society of Cardiology
The role of V2 vasopressin antagonists in hyponatremia
Department of Medicine, Division of Nephrology, Universitätsklinikum C.G. Carus, Dresden, Germany
* Corresponding author. Nephrology, MK III, U.K.D., Fetscherstrasse 76, 01307 Dresden, Germany peter.gross{at}tu-dresden.de
Hyponatremia is a frequent electrolyte disorder. It is often found in congestive cardiac failure, liver cirrhosis, plasma volume contraction and in SiADH. In these disorders hyponatremia is caused by nonosmotic vasopressin and sustained fluid intake. This provides a rationale for V2 vasopressin receptor antagonists in the treatment of hyponatremia. There is now convincing evidence from different animal models of congestive cardiac failure that peptide and non-peptide V2 vasopressin antagonists effectively increase renal water diuresis and plasma sodium concentration. In addition, several of the experimental studies also showed an improvement of hemodynamic changes of cardiac failure in response to V2 antagonists. Data in patients indicated that oral non-peptide V2-antagonists correct hyponatremia and may improve hemodynamic derangements in cardiac failure. In addition, experimental and clinical studies of V2 antagonists have been undertaken in liver cirrhosis and SiADH. In those studies hyponatremia was improved or corrected, too. Taken together, V2 vasopressin antagonists promise to become therapeutic agents in hyponatremic disorders.
KEYWORDS ANP, atrial natriuretic peptide; AQP, aquaporin water channel protein; CCF, congestive heart failure; CD, for collecting duct; GFR, glomerular filtration rate; MAP, mean arterial blood pressure; NDI, nephrogenic diabetes insipidus; PCWP, pulmonary capillary wedge pressure; RAP, right atrial pressure; SIADH, syndrome of inappropriate antidiuretic hormone; V2 R, vasopressin V2 receptor; VSMC, vascular smooth muscle cells
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