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Endocrinology Vol. 141, No. 1 307-314
Copyright © 2000 by The Endocrine Society

ARTICLES

Vasopressin V2 Receptor Binding Is Down-Regulated during Renal Escape from Vasopressin-Induced Antidiuresis1

Ying Tian, Kathryn Sandberg, Takashi Murase, Erin A. Baker, Robert C. Speth and Joseph G. Verbalis

Divisions of Endocrinology and Metabolism, and Nephrology, Department of Medicine, Georgetown University (Y.T., K.S., T.M., E.A.B., J.G.V.), Washington, D.C. 20007; and the School of Veterinary Medicine, Washington State University (R.C.S.), Pullman, Washington 99164

Address all correspondence and requests for reprints to: Dr. Joseph G. Verbalis, 232 Building D, Georgetown University, 4000 Reservoir Road NW, Washington, D.C. 20007. E-mail: verbalis{at}gunet.georgetown.edu

This study evaluated whether renal escape from vasopressin-induced antidiuresis is associated with alterations of vasopressin V2 receptor binding in the kidney inner medulla. A radioligand binding assay was developed using a novel iodinated vasopressin V2 receptor antagonist to analyze vasopressin V2 receptor binding in kidney inner medullary tissue from three groups of rats: normal rats maintained on ad libitum water intake, rats treated with 1-deamino-[8-D-arginine]vasopressin (DDAVP), and rats treated with DDAVP that were also water loaded to induce renal escape from antidiuresis. Analysis of the binding data showed that DDAVP treatment reduced vasopressin V2 receptor binding to 72% of normal levels. Water loading induced a marked further down-regulation of vasopressin V2 receptor binding. This receptor down-regulation began by day 2 of water loading, which correlated with the initiation of renal vasopressin escape; by day 3 of water loading, vasopressin V2 receptor expression fell to 43% of DDAVP-treated levels. No differences in vasopressin V2 receptor binding affinities were found among the three groups. This study demonstrates that vasopressin V2 receptor binding capacity is down-regulated during renal escape from vasopressin-induced antidiuresis and suggests that both vasopressin-dependent mechanisms as well as vasopressin-independent mechanisms associated with water loading are involved in this receptor down-regulation.




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