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TRANSLATIONAL PHYSIOLOGY

Effects of terlipressin on the aquaretic system: evidence of antidiuretic effects

Departments of ¹Gastroenterology and ²Clinical Physiology, Hvidovre University Hospital, Faculty of Health Sciences, University of Copenhagen, Hvidovre; ³Department of Medical Research and Department of Medicine, Holstebro Hospital, Holstebro; and ⁴Department of Biomedical Sciences, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark

Submitted 11 July 2008 ; accepted in final form 20 August 2008

The vasopressin analog terlipressin is believed to cause vasoconstriction selectively by V₁ receptor stimulation. However, a possible antidiuretic effect by V₂ receptor stimulation has never been ruled out. Twenty-two patients with ascites, including seven with refractory ascites, were included. The subjects were studied during a 400 ml/h oral water load before and after infusion of 2 mg of terlipressin (18 patients) or placebo infusion (4 patients). Effects on the V₂ receptors were assessed by evaluating aquaporin (AQP)2 excretion, free water clearance (C), urine osmolality (U_osm), and fractional distal water excretion (DFeH₂O). After terlipressin the excretion of AQP2 increased by 89% [144 ng/mmol creatinine, 95% confidence interval (CI) 73–214 ng/mmol creatinine, P = 0.001]. C decreased 1.05 ml/min (from 0.17 to –0.89 ml/min, P = 0.001), and DFeH₂O decreased 37% (19 vs. 12; 95% CI 2–11, P = 0.01). U_osm increased by 27% (93 mosmol/kgH₂O, 95% CI 23–164 mosmol/kgH₂O, P = 0.02). Plasma sodium decreased 1.1 mmol/l (P < 0.01). An increase in AQP2 excretion and a decrease in C and distal water excretion after terlipressin despite water loading is a clear indication of activation of the antidiuretic system (V₂ receptor effect).

aquaporin-2; vasopressin; hepatorenal syndrome; cirrhosis; ascites

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