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Am J Physiol Renal Physiol (January 23, 2007). doi:10.1152/ajprenal.00300.2006
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Submitted on August 1, 2006
Accepted on January 16, 2007

The mobilization of osmotically inactive Na+ by growth and by dietary salt restriction in rats

Markus Schafflhuber1, Nicola Volpi2, Anke Dahlmann1, Karl F. Hilgers1, Francesca Maccari2, Peter Dietsch3, Hubertus Wagner4, Friedrich C. Luft5, Kai-Uwe Eckardt1, and Jens Titze1*

1 Nephrology and Hypertension, Friedrich-Alexander-University Erlangen-Nürnberg, Germany
2 Department of Animal Biology, University of Modena & Reggio Emilia, Italy
3 Biochemistry, Charite, Campus Benjamin Franklin, Berlin, Germany
4 Chemistry, Federal Centre for Nutrition and Food, Kulmbach, Germany
5 Franz Volhard Clinic, HELIOS Klinikum-Berlin and, Charite, Campus Buch, Berlin, Germany

* To whom correspondence should be addressed. E-mail: jens.titze{at}rzmail.uni-erlangen.de.

The idea that an osmotically inactive Na+ storage pool exists that can be varied to accommodate states of Na+ retention and/or Na+ loss is controversial. We speculated that considerable amounts of osmotically inactive Na+ are lost with growth and that additional dietary salt excess or salt deficit alters the polyanionic character of extracellular glycosaminoglycans in osmotically inactive Na+ reservoirs. Six week-old Sprague-Dawley rats were fed low-salt (0.1%; LS) or high-salt (8%; HS) diets for 1 or 4 weeks. At sacrifice, we separated the tissues and determined their Na+, K+, and water content. Three weeks of growth reduced the total body Na+ content relative to dry weight (rTBNa+) by 23%. This "growth programmed" Na+ loss originated mainly from the bone and the completely skinned and bone-removed carcasses. The Na+ loss was osmotically inactive (45-50%), or osmotically active (50-55%). In rats aged 10 weeks, compared to HS, 4 weeks LS reduced rTBNa+ by 9%. This dietary-induced Na+ loss was osmotically inactive ({approx}50%) and originated largely from the skin, while {approx}50% was osmotically active. LS for 1 week did not reduce skin Na+ content. The mobilization of osmotically inactive skin Na+ with long-term salt deprivation was associated with decreased negative charged skin glycosaminoglycan content and thereby a decreased water-free Na+ binding capacity in the extracellular matrix. Our data not only serve to explain discrepant results in salt balance studies, but also show that glycosaminoglycans may provide an actively regulated interstitial cation exchange mechanism that participates in volume and blood pressure homeostasis.




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