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Nephrol Dial Transplant (1999) 14: 2559-2562
© 1999 European Renal Association-European Dialysis and Transplant Association


Editorial Comments

V2-vasopressin receptor antagonists—mechanism of effect and clinical implications in hyponatraemia

Catrin Palm and Peter Gross

Division of Nephrology, Department of Medicine, Universitätsklinikum C. G. Carus, Dresden, FRG

Correspondence and offprint requests to: Dr Catrin Palm, Division of Nephrology, Department of Medicine, Universitätsklinikum C. G. Carus, Fetscherstr. 74, D-01307 Dresden, FRG.

Keywords: cardiac failure; liver cirrhosis; syndrome of inappropriate antidiuretic hormone secretion; treatment of hyponatraemia; vasopressin; vasopressin receptor antagonists

Introduction

Hyponatraemia (serum sodium <135 mmol/l) is the most frequent electrolyte disturbance in clinical practice. Its clinical relevance is related to both the symptoms it causes and the state of cardiovascular dysfunction it indicates. Hyponatraemic patients may suffer from lethargy, difficulty of concentration, disorientation, muscular cramps, grand mal seizures, and even coma. It is important to know that these symptoms are more related to the rate of decrease of serum sodium concentration than to the absolute level of a hyponatraemia reached. This surprising observation is related to the phenomenon of osmotic unloading of cells, which causes adaptation of cell volume to any given degree of hyponatraemia within 2–4 days. Osmotic reloading will have to occur during correction of hyponatraemia. Since this will take a similar amount of time to be completed, the rate of correction of hyponatraemia should not be in excess of 0.5 mmol/l/h. If chronic hyponatraemia is corrected too . . . [Full Text of this Article]

Pathophysiological significance of hyponatraemia

Significance of hydro-osmotic V2-vasopressin receptors

Pharmacology of vasopressin V2 receptor antagonists

Studies of vasopressin V2 antagonists in cardiac failure

Studies of vasopressin V2 antagonists in liver cirrhosis

Studies of V2 vasopressin antagonists in SIADH

Conclusions

References


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