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

New FindingsWhat 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.