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Acta Physiologica Congress

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Acta Physiologica 2006; Volume 187, Supplement 659
The Scandinavian Physiological Society's Annual Meeting
8/11/2006-8/13/2006
Reykjavik, Iceland


NON-OSMOTIC SODIUM STORAGE AS A MECHANISM FOR BLOOD PRESSURE CONTROL
Abstract number: 1501

HEER1 M, FRINGS1 P, BECK1 L

1German Aerospace Center (DLR), Institute of Aerospace Medicine, Linder Hoehe, Koeln, Germany [email protected]

We have recently shown that high salt intake may lead to sodium retention without fluid retention (Heer et al. 2000), called osmotically inactive sodium retention (Farber et al. 1957). To distinguish between effects when starting from a low to high salt intake and from a high to an even higher intake we examined nine healthy, male test subjects. They received 50 mEq/d NaCl (Phase 1), 200 mEq/d (Phase 2), 550 mEq/d NaCl (Phase 3) and again 50 mEq/d NaCl again (Phase 4) in four consecutive study phases. Body weight (BW) increased significantly from phase 1 to phase 2 and further increased to phase 3. Reduction of salt intake in phase 4 led to a BW-loss. PV and ECV increased significantly from phase 1 to 2, but did not further increase from phase 2 to 3. During phase 4, PV and ECV reached the volumes of phase 1. Cumulative water balance showed fluid losses in phase 1, fluid retention in phase 2, fluid loss in phase 3 and further losses in phase 4. Cumulative sodium balance showed sodium loss in phase 1, sodium retention in phase 2 and phase 3 and sodium loss in phase 4. Urinary potassium excretion increased from phase 1 to phase 2. In phase 3 the level of phase 2 was kept and decreased in the 4th study phase. We conclude that increasing salt intake leads first to an osmotic active and then to an osmotic inactive sodium retention. This might be important in blood pressure regulation.

To cite this abstract, please use the following information:
Acta Physiologica 2006; Volume 187, Supplement 659 :1501

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