Na⁺ is shifted from the extracellular to the intracellular compartment and is not inactivated by glycosaminoglycans during high salt conditions in rats

Abstract

Abstract Recently, studies have emerged suggesting that the skin plays a role as major Na + reservoir via regulation of the content of glycosaminoglycans and osmotic gradients. We investigated whether there were electrolyte gradients in skin and where Na + could be stored to be inactivated from a fluid balance viewpoint. Na + accumulation was induced in rats by a high salt diet (HSD) (8% NaCl and 1% saline to drink) or by implantation of a deoxycorticosterone acetate (DOCA) tablet (1% saline to drink) using rats on a low salt diet (LSD) (0.1% NaCl) on tap water as control. Na + and K + were assessed by ion chromatography in tissue eluates, and the extracellular volume by equilibration of 51 Cr‐EDTA. By tangential sectioning of the skin, we found a low Na + content and extracellular volume in epidermis, both parameters rising by ∼30% and 100%, respectively, in LSD and even more in HSD and DOCA when entering dermis. We found evidence for an extracellular Na + gradient from epidermis to dermis shown by an estimated concentration in epidermis ∼2 and 4–5 times that of dermis in HSD and DOCA‐salt. There was intracellular storage of Na + in skin, muscle, and myocardium without a concomitant increase in hydration. Our data suggest that there is a hydration‐dependent high interstitial fluid Na + concentration that will contribute to the skin barrier and thus be a mechanism for limiting water loss. Salt stress results in intracellular storage of Na + in exchange with K + in skeletal muscle and myocardium that may have electromechanical consequences. Key points Studies have suggested that Na + can be retained or removed without commensurate water retention or loss, and that the skin plays a role as major Na + reservoir via regulation of the content of glycosaminoglycans and osmotic gradients. In the present study, we investigated whether there were electrolyte gradients in skin and where Na + could be stored to be inactivated from a fluid balance viewpoint. We used two common models for salt‐sensitive hypertension: high salt and a deoxycorticosterone salt diet. We found a hydration‐dependent high interstitial fluid Na + concentration that will contribute to the skin barrier and thus be a mechanism for limiting water loss. There was intracellular Na + storage in muscle and myocardium without a concomitant increase in hydration, comprising storage that may have electromechanical consequences in salt stress.

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