HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 295/5/F1295    most recent 90407.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Krag, A. Articles by Møller, S. Search for Related Content PubMed PubMed Citation Articles by Krag, A. Articles by Møller, S.

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

This article has been cited by other articles:

				W. A. Hackworth and A. J. Sanyal Review: Vasoconstrictors for the treatment of portal hypertension Therapeutic Advances in Gastroenterology, March 1, 2009; 2(2): 119 - 131. [Abstract] [PDF]