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Molecular Mechanisms of Antidiuretic Effect of Oxytocin

Chunling Li^*, Weidong Wang^*, Sandra N. Summer^*, Timothy D. Westfall, David P. Brooks, Sandor Falk^* and Robert W. Schrier^*

^* Department of Medicine, University of Colorado School of Medicine, Denver, Colorado; and Department of Urogenital Biology, GlaxoSmithKline Research and Development, King of Prussia, Pennsylvania

Correspondence: Robert W. Schrier, MD, Division of Renal Diseases and Hypertension, University of Colorado Health Sciences Center, 4200 East 9th Avenue, Box B173, Denver, CO 80262. Phone: 303-315-8059; Fax: 303-315-2685; E-mail: Robert.Schrier{at}UCHSC.edu

Received for publication January 8, 2007. Accepted for publication August 7, 2007.

Oxytocin is known to have an antidiuretic effect, but the mechanisms underlying this effect are not completely understood. We infused oxytocin by osmotic minipump into vasopressin-deficient Brattleboro rats for five days and observed marked antidiuresis, increased urine osmolality, and increased solute-free water reabsorption. Administration of oxytocin also significantly increased the protein levels of aquaporin-2 (AQP2), phosphorylated AQP2 (p-AQP2), and AQP3 in the inner medulla and in the outer medulla plus cortex. Immunohistochemistry demonstrated increased AQP2 and p-AQP2 expression and trafficking to the apical plasma membrane of principal cells in the collecting duct, and increased AQP3 expression in the basolateral membrane. These oxytocin-induced effects were blocked by treatment with the vasopressin V2 receptor antagonist SR121463B, but not by treatment with the oxytocin receptor antagonist GW796679X. We conclude that vasopressin V2 receptors mediate the antidiuretic effects of oxytocin, including increased expression and apical trafficking of AQP2, p-AQP2, and increased AQP3 protein expression.

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Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673