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

Abstract

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.

Cyclooxygenase-2 Modulates Glycosaminoglycan Production in the Skin During Salt Overload

“…The amount of skin Na + -binding GAGs positively correlates with skin Na + content (Fischereder et al, 2017;Sugar et al, 2018). High salt consumption increases Na + content as well as the amount of GAGs of the skin (Titze et al, 2003(Titze et al, , 2004, while in salt depletion, both of them decrease (Schafflhuber et al, 2007;Sugar et al, 2018;Lopes-Menezes et al, 2019). Consensus holds that the Na + storage mediated by GAGs is an actively regulated process.…”

Rethinking furosemide use for infants with bronchopulmonary dysplasia

“…These pools consist of sodium bound to negatively charged glycosaminoglycan within the skin interstitium 16 . Factors regulating the storage and release of sodium from these pools have not been elucidated, though, in animal studies, furosemide mobilizes and depletes skin sodium stores 17 …”

Neurobehavioral Mechanisms of Sodium Appetite

“…One resolution of the time course issues would be the existence of a slow-depleting and -repleting sodium reservoir. While the older literature failed to identify such a reservoir—please see [ 8 ] and [ 12 ] for citations and discussion—, the skin [ 17 ] and bone [ 18 ] have now emerged as viable candidates.…”