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Atrap Deficiency Increases Arterial Blood Pressure and Plasma Volume

Mona Oppermann^*, Bernhard Gess, Frank Schweda and Hayo Castrop

*Children's Hospital, University Medical Center, and
Institute of Physiology, University of Regensburg, Regensburg, Germany

Correspondence: Dr. Hayo Castrop, Institute of Physiology, University of Regensburg, Universitätsstrasse 31, 93040 Regensburg, Germany. Phone: +49-941-943-2967; Fax: +49-941-943-4315; E-mail: hayo{at}castrop.com

Received for publication November 11, 2009. The angiotensin receptor-associated protein (Atrap) interacts with angiotensin II (AngII) type 1 (AT1) receptors and facilitates their internalization in vitro, but little is known about the function of Atrap in vivo. Here, we detected Atrap expression in several organs of wild-type mice; the highest expression was in the kidney where it localized to the proximal tubule, particularly the brush border. There was no Atrap expression in the renal vasculature or juxtaglomerular cells. We generated Atrap-deficient (Atrap–/–) mice, which were viable and seemed grossly normal. Mean systolic BP was significantly higher in Atrap–/– mice compared with wild-type mice. Dose-response relationships of arterial BP after acute AngII infusion were similar in both genotypes. Plasma volume was significantly higher and plasma renin concentration was markedly lower in Atrap–/– mice compared with wild-type mice. ¹²⁵I-AngII binding showed enhanced surface expression of AT1 receptors in the renal cortex of Atrap–/– mice, accompanied by increased carboanhydrase-sensitive proximal tubular function. In summary, Atrap–/– mice have increased arterial pressure and plasma volume. Atrap seems to modulate volume status by acting as a negative regulator of AT1 receptors in the renal tubules.

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Copyright © 2009 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673