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Am J Physiol Renal Physiol 289: F793-F802, 2005. First published May 24, 2005; doi:10.1152/ajprenal.00096.2005
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Internal sodium balance in DOCA-salt rats: a body composition study

Jens Titze,1 Katharina Bauer,1 Markus Schafflhuber,1 Peter Dietsch,2 Rainer Lang,1 Karl H. Schwind,3 Friedrich C. Luft,4 Kai-Uwe Eckardt,1 and Karl F. Hilgers1

1Department of Nephrology and Hypertension, Friedrich-Alexander-University, Erlangen-Nürnberg, Germany; 2Institute of Biochemistry, Charité Campus Benjamin Franklin, Berlin, Germany; 3Federal Center for Meat Research, Kulmbach, Germany; and 4Charité Campus Buch, Franz Volhard Clinic, HELIOS Klinikum-Berlin and Max Delbrück Center for Molecular Medicine, Berlin, Germany

Submitted 9 March 2005 ; accepted in final form 16 May 2005

The idea that Na+ retention inevitably leads to water retention is compelling; however, were Na+ accumulation in part osmotically inactive, regulatory alternatives would be available. We speculated that in DOCA-salt rats Na+ accumulation is excessive relative to water. Forty female Sprague-Dawley rats were divided into four subgroups. Groups 1 and 2 (controls) received tap water or 1% saline (salt) for 5 wk. Groups 3 and 4 received subcutaneous DOCA pellets and tap water or salt. Na+, K+, and water were measured in skin, bone, muscle, and total body by desiccation and consecutive dry ashing. DOCA-salt led to total body Na+ excess (0.255 ± 0.022 vs. 0.170 ± 0.010 mmol/g dry wt; P < 0.001), whereas water retention was only moderate (0.685 ± 0.119 vs. 0.648 ± 0.130 ml/g wet wt; P < 0.001). Muscle Na+ retention (0.220 ± 0.029 vs. 0.145 ± 0.021 mmol/g dry wt; P < 0.01) in DOCA-salt was compensated by muscle K+ loss, indicating osmotically neutral Na+/K+ exchange. Skin Na+ retention (0.267 ± 0.049 vs. 0.152 ± 0.014 mmol/g dry wt; P < 0.001) in DOCA-salt rats was not balanced by K+ loss, indicating osmotically inactive skin Na+ storage. We conclude that DOCA-salt leads to tissue Na+ excess relative to water. The relative Na+ excess is achieved by two distinct mechanisms, namely, osmotically inactive Na+ storage and osmotically neutral Na+ retention balanced by K+ loss. This "internal Na+ escape" allows the maintenance of volume homeostasis despite increased total body Na+.

hypertension; sodium storage; hypertensive rats; mineralocorticoid escape


Address for reprint requests and other correspondence: J. Titze, Forschungslabor der Medizinischen Klinik IV, Kreuzburger Strasse 2, 90471 Nürnberg, Germany (e-mail: jens.titze{at}rzmail.uni-erlangen.de)




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