Reduced osmotically inactive Na storage capacity and hypertension in the Dahl model

Author:

Titze Jens1,Krause Holger1,Hecht Hermann2,Dietsch Peter3,Rittweger Jörn4,Lang Rainer1,Kirsch Karl A.4,Hilgers Karl F.1

Affiliation:

1. Department of Nephrology, Friedrich-Alexander-University Erlangen-Nürnberg, D-91054 Erlangen;

2. Department of Chemistry and Physics, Federal Center for Meat Research, D-95326 Kulmbach; and Departments of

3. Biochemistry and

4. Physiology, Free University of Berlin, D-14195 Berlin, Germany

Abstract

Recent evidence suggested that Na can be stored in an osmotically inactive form. We investigated whether osmotically inactive Na storage is reduced in a rat model of salt-sensitive (SS) hypertension. SS and salt-resistant (SR) Dahl-Rapp rats as well as Sprague-Dawley (SD) rats were fed a high (8%)- or low (0.1%)-NaCl diet for 4 wk ( n = 10/group). Mean arterial pressure (MAP) was measured at the end of the experiment. Wet and dry weights, water content, total body Na (TBS), and bone Na content were measured by dessication and dry ashing. MAP was higher in both Dahl strains than in SD rats. In SS rats, 8% NaCl led to Na accumulation, water retention, and hypertension due to impaired renal Na excretion. There was no dietary-induced Na retention in SR and SD rats. TBS was variable; nevertheless, TBS was significantly correlated with body water and MAP in all strains. However, the extent of Na-associated volume and MAP increases was strain specific. Osmotically inactive Na in SD rats was threefold higher than in SS and SR rats. Both SS and SR Dahl rat strains displayed reduced osmotically inactive Na storage capacity compared with SD controls. A predisposition to fluid accumulation and high blood pressure results from this alteration. Additional factors, including impaired renal Na excretion, probably contribute to hypertension in SS rats. Our results draw attention to the role of osmotically inactive Na storage.

Publisher

American Physiological Society

Subject

Physiology

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