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Am J Physiol Renal Physiol 287: F160-F168, 2004. First published March 9, 2004; doi:10.1152/ajprenal.00329.2003
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Opioid receptor-like 1 stimulation in the collecting duct induces aquaresis through vasopressin-independent aquaporin-2 downregulation

Niels Hadrup,1 Jørgen S. Petersen,2 Jeppe Praetorius,3 Eddi Meier,2 Martin Græbe,1 Lone Brønd,1 Dennis Staahltoft,1 Søren Nielsen,3 Sten Christensen,1 Daniel R. Kapusta,4 and Thomas E. N. Jonassen1

1Department of Pharmacology, University of Copenhagen, DK-2200 Copenhagen N; 2Zealand Pharma, DK-2600 Glostrup; 3The Water and Salt Research Center, Institute of Anatomy, University of Aarhus, DK-8000 Aarhus, Denmark; and 4Department of Pharmacology and Experimental Therapeutics and Neuroscience Center of Excellence, Louisiana State University Health Sciences Center, New Orleans, Louisiana 70112

Submitted 11 August 2003 ; accepted in final form 3 March 2004

Nociceptin, the endogenous ligand of the inhibitory G protein-coupled opioid receptor-like 1 receptor, produces aquaresis (i.e., increases the excretion of solute-free urine) in rats. However, the mechanism underlying this effect has not yet been explained. Using immunohistochemistry, we found the opioid receptor-like 1 receptor in the rat kidney colocalized with the vasopressin-regulated water channel aquaporin-2 in inner medullary collecting ducts. We investigated the aquaretic effect of opioid receptor-like 1 receptor stimulation by infusing the selective nociceptin analog ZP120C; volume depletion was prevented by computer-driven, servo-controlled intravenous volume replacement with 50 mM glucose. ZP120C induced a marked and sustained aquaresis in normal and congestive heart failure rats in the absence of changes in vasopressin plasma concentrations. The ZP120C-induced aquaresis was associated with downregulation of the aquaporin-2 protein level in both rat groups, suggesting that opioid receptor-like 1 receptor stimulation produces aquaresis by inhibiting the vasopressin type-2 receptor-mediated stimulation on collecting duct water reabsorption. However, substantial amounts of PKA-mediated serine 256 phosphorylated aquaporin-2 were still present after 4 h of ZP120C treatment. Furthermore, neither preincubation with nociceptin nor ZP120C inhibited vasopressin-mediated cAMP accumulation in isolated collecting ducts. We conclude that renal opioid receptor-like 1 receptor stimulation in normal and congestive heart failure rats produces aquaresis by a direct renal effect, via aquaporin-2 downregulation, through a mechanism not involving inhibition of vasopressin type-2 receptor-mediated cAMP production.

nociceptin; ZP120C; phosphorylated aquaporin-2; congestive heart failure


Address for reprint requests and other correspondence: N. Hadrup, Dept. of Pharmacology, Univ. of Copenhagen, Blegdamsvej 3, 2200 Copenhagen N, Denmark (E-mail: niels.hadrup{at}farmakol.ku.dk).




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