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Water deprivation-induced sodium appetite: humoral and cardiovascular mediators and immediate early genes
Journal article   Open access   Peer reviewed

Water deprivation-induced sodium appetite: humoral and cardiovascular mediators and immediate early genes

Laurival A De Luca, Zhice Xu, Guus H. M Schoorlemmer, Robert L Thunhorst, Terry G Beltz, José V Menani and Alan Kim Johnson
American journal of physiology. Regulatory, integrative and comparative physiology, Vol.282(2), pp.R552-R559
02/01/2002
DOI: 10.1152/ajpregu.00295.2000
PMID: 11792666
url
https://doi.org/10.1152/ajpregu.00295.2000View
Published (Version of record) Open Access

Abstract

10.1152/ajpregu.00295.2000. Adult rats deprived of water for 24–30 h were allowed to rehydrate by ingesting only water for 1–2 h. Rats were then given access to both water and 1.8% NaCl. This procedure induced a sodium appetite defined by the operational criteria of a significant increase in 1.8% NaCl intake (3.8 ± 0.8 ml/2 h; n = 6). Expression of Fos (as assessed by immunohistochemistry) was increased in the organum vasculosum of the lamina terminalis (OVLT), median preoptic nucleus (MnPO), subfornical organ (SFO), and supraoptic nucleus (SON) after water deprivation. After rehydration with water but before consumption of 1.8% NaCl, Fos expression in the SON disappeared and was partially reduced in the OVLT and MnPO. However, Fos expression did not change in the SFO. Water deprivation also 1) increased plasma renin activity (PRA), osmolality, and plasma Na+; 2) decreased blood volume; and 3) reduced total body Na+; but 4) did not alter arterial blood pressure. Rehydration with water alone caused only plasma osmolality and plasma Na+concentration to revert to euhydrated levels. The changes in Fos expression and PRA are consistent with a proposed role for ANG II in the control of the sodium appetite produced by water deprivation followed by rehydration with only water.

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