Acute body sodium depletion induces skin sodium mobilization in female Wistar rats

New findings: What is the central question of this study? Can Na⁺ depletion mobilize Na⁺ from the skin reservoir in ovariectomized rats? Does oestrogen replacement change the amount and the dynamics of skin Na⁺ storage? Is the reduced salt appetite after Na⁺ depletion in ovariectomized rats with oestrogen replacement related to changes in the skin Na⁺ ? What is the main finding and its importance? This work demonstrated that acute body Na⁺ depletion induced by frusemide mobilized the osmotically inactive skin Na⁺ reservoir to become osmotically active. Oestrogen treatment decreased the induced Na⁺ intake in ovariectomized rats but did not modulate the inactive Na⁺ reservoir in control conditions or its mobilization induced by Na⁺ depletion.

Abstract: Oestradiol, which is an important hormone for water and electrolyte balance, also has a role in the inhibition of induced Na⁺ appetite. Sodium can be stored in the skin in osmotically active or inactive forms, and this skin Na⁺ reservoir may be involved in the control of body Na⁺ levels during physiopathological challenges. In this study, we investigated whether the effect of sodium depletion by frusemide can mobilize Na⁺ from the skin reservoir and whether oestradiol replacement changes or mobilizes the Na⁺ reserves in the skin. Ovariectomized Wistar rats were treated with vehicle or oestradiol for 7 days to evaluate the effects of oestrogen on the hydroelectrolyte balance, intake responses and skin Na⁺ and water content in basal conditions. Furthermore, the effects of oestrogen were evaluated after 24 h frusemide-induced whole-body Na⁺ depletion. Oestradiol-replaced rats exhibited reduced water intake without any significant changes in salt intake, Na⁺ excretion or water and Na⁺ skin content in basal conditions. After sodium depletion, both vehicle- and oestradiol-treated rats exhibited an increase in the osmotically active skin Na⁺ , which was associated with a decrease of the inactive skin Na⁺ reservoir. Oestrogen decreased the hypertonic saline intake induced by Na⁺ depletion, but it was not associated with any significant changes in the skin Na⁺ reservoir. Thus, sodium depletion is able to change the inactive-active skin Na⁺ reservoir balance. However, the oestrogenic modulation of sodium appetite after Na⁺ depletion is probably not related to the action of this hormone in the skin Na⁺ reservoir balance.