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

Abstract

. Water deprivation-induced sodium appetite: humoral and cardiovascular mediators and immediate early genes. Am J Physiol Regulatory Integrative Comp Physiol 282: R552-R559, 2002; 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 Ϯ 0.8 ml/2 h; n ϭ 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 ϩ ; 2) decreased blood volume; and 3) reduced total body Na ϩ ; but 4) did not alter arterial blood pressure. Rehydration with water alone caused only plasma osmolality and plasma Na ϩ 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. salt intake; hypovolemia; circumventricular organs; dehydration; thirst MODELS OF NA ϩ INGESTION based on selective depletion of the extracellular fluid compartment have revealed several potential mechanisms that control Na ϩ ingestion. These models typically employ combinations of Na ϩ deprivation and depletion to induce hypovolemia. In the rat, Na ϩ ingestion after Na ϩ loss in these models is associated with increased levels of circulating ANG II and aldosterone (9), unloading of baroreceptors (20), and inhibition of oxytocin secretion by dilution of body fluids after the Na ϩ -depleted animals have ingested water (42). Water deprivation is another procedure associated with an increased preference for ingesting NaCl solutions (48). During water deprivation, the obligatory excretion of water coupled with increased natriuresis results in dehydration of both the intracellular and extracellular fluid compartments (21,25,35). Like selective extracellular depletion models of Na ϩ ingestion, water deprivation reduces blood volume and increases plasma renin activity (PRA) and levels of circulating ANG II (8,29,30,35). However, in contrast to the selective extracellular dehydration models, water deprivation is accompanied by reductions, or no changes, in plasma levels of aldosterone (29,34) and by increases in plasma Na ϩ concentration ([Na ϩ ]) and osmolality (29,34,35 ] and osmolality levels are reduced after dehydrated animals drink water.Water-deprived animals clearly prefer to drink water, but there is also considerable ingestion of hypertonic saline solutions wh...

Mechanisms of brain renin angiotensin system-induced drinking and blood pressure: importance of the subfornical organ

“…Similarly, elevating blood-borne ANG II either exogenously or indirectly by decreasing blood pressure via isoproterenol increases neuronal activity, the expression of AT 1 R within the SFO, and water intake (57,69,115). Fluid restriction also increases the expression of c-Fos (i.e., an indirect indicator of cellular activity) within the SFO, which remains elevated immediately after rehydration, whereas in other nuclei, c-Fos expression returns to normal (25). Table 2 summarizes stimuli that influence fluid intake and involve the SFO.…”

Water deprivation-partial rehydration induces sensitization of sodium appetite and alteration of hypothalamic transcripts

“…Animals were deprived of both water (WD) and 0.3 M NaCl, but maintained free access to regular food in their cages, for 36 h (experiment 1) or 24 h (experiment 2), according to previous studies (5,32). In sequence, animals were weighed and returned to their cages, from which food had been removed, and a glass burette (with 0.1-ml divisions fitted with a stainless-steel spout) containing filtered water was offered for 2 h to allow a partial extracellular volume repletion, or partial rehydration (PR) condition.…”

“…The WD-PR is a useful experimental protocol to separate thirst from sodium appetite in water-deprived rats (5,6,38), and possibly in humans (16). The PR period, characterized by full restoration of plasma osmolality, but only partial restoration of the extracellular fluid volume, is attained through ingestion of only water to satiety in a thirst test performed at the end of a cycle of WD.…”

“…The PR period, characterized by full restoration of plasma osmolality, but only partial restoration of the extracellular fluid volume, is attained through ingestion of only water to satiety in a thirst test performed at the end of a cycle of WD. The sodium appetite is then expressed by ingestion of NaCl solution in a sodium appetite test performed immediately after the thirst test, thus restoring sodium balance and extracellular volume (5). The ingestion of NaCl in the sodium appetite test is a behavior that results from the production of transient negative sodium balance because of the obligatory sodium loss in urine during dehydration (5).…”

“…The sodium appetite is then expressed by ingestion of NaCl solution in a sodium appetite test performed immediately after the thirst test, thus restoring sodium balance and extracellular volume (5). The ingestion of NaCl in the sodium appetite test is a behavior that results from the production of transient negative sodium balance because of the obligatory sodium loss in urine during dehydration (5). Because of the sodium loss, the behavior also depends on the production of the neuropeptide ANG II and activation of its receptor type 1, the AT 1 receptor (38).…”