Role of sodium concentration of the cerebrospinal fluid in the salt appetite of sheep

Weisinger, R. S.; Considine, P. J.; Denton, D. A.; Leksell, L; McKinley, MJ; Mouw, David R.; Müller, Alex F.; Tarján, É.

doi:10.1152/ajpregu.1982.242.1.r51

Cited by 38 publications

(32 citation statements)

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“…Under similar conditions the sodium intake of sodium-replete sheep increased also (Weisinger et al 1982). In the wild rabbit, infusion of 0 9 M-mannitol c.s.f.…”

Section: Discussionmentioning

confidence: 82%

Water and salt intake of wild rabbits (Oryctolagus cuniculus (L)) following dipsogenic stimuli.

Denton¹,

Nelson²,

Tarján³

1985

The Journal of Physiology

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SUMMARY1. Wild rabbits trapped in their natural habitat and adapted to laboratory conditions were studied. Food, water and electrolyte (0-5 M-NaCl, 0-5 M-KCl, 0-25 M-MgCl2 and 0-25 M-CaCl2) consumption, urinary volume and sodium losses were monitored daily following stimuli which were found dipsogenic in other species.2. Water drinking was observed immediately after the intravenous injection of 1 M-NaCl (3 ml/kg), and following withdrawal of a mean of 13-9 % of calculated blood volume. Daily intake of water decreased during intracerebroventricular (i.c.v.) infusion of 0 3 M-NaCl in artificial cerebrospinal fuid (c.s.f.), during i.c.v. infusion of 0 9 M-mannitol c.s.f., both at a rate of 17 1d/h, following peritoneal dialysis with 5 % (w/v) glucose solution, and during food restriction. Water intake was not affected following intravenous administration of acetazolamide (10 mg/kg).3. Daily intake of 0'5 M-NaCl solution was increased following peritoneal dialysis with 5 % (w/v) glucose solution, which caused hyponatraemia, but not after haemorrhage which caused about the same sodium deficit as peritoneal dialysis, but as an isosmotic loss. 4. Administration of two different angiotensin II analogues, systemically or i.c.v., failed to induce water drinking. However, urinary sodium excretion and intake of 05 M-NaCl were increased during the 5 days of i.c.v. infusion of angiotensin II (10 pmol/h). Infusion for 1 day of angiotensin II (500 pmol/h) led to increased urinary sodium excretion which was followed by increased intake.5. The intake of other electrolyte solutions was not significantly affected by any of the treatments detailed above.6. The mechanisms participating in initiation of thirst in wild rabbits are very sensitive to decrease in blood volume, in contrast to other species studied in laboratories. Angiotensin II at the doses and routes administered was not dipsogenic in wild rabbits.7. The increased intake of 05 M-NaCl solution observed during and after the long-term intraventricular administration of angiotensin II in the wild rabbit appears predominantly a response to sodium deficit caused by natriuresis. The persistence of appetite after the cessation of infusion is indicative of a residual effect on central mechanisms of salt appetite.

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“…Under similar conditions the sodium intake of sodium-replete sheep increased also (Weisinger et al 1982). In the wild rabbit, infusion of 0 9 M-mannitol c.s.f.…”

Section: Discussionmentioning

confidence: 82%

Water and salt intake of wild rabbits (Oryctolagus cuniculus (L)) following dipsogenic stimuli.

Denton¹,

Nelson²,

Tarján³

1985

The Journal of Physiology

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“…Osmolality and [Na ϩ ] of the cerebrospinal fluid may also increase during water deprivation (5), and this might contribute to the inhibition of sodium appetite (4,5,7,46). The inhibition arising from hyperosmolality and hypernatremia is then reduced when rats ingest water during the rehydration phase.…”

Section: Discussionmentioning

confidence: 99%

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

Luca

Schoorlemmer

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

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. 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...

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“…Under sodium deprivation conditions, animals display an increase in the salt intake over a wide range of sodium chloride concentrations (Weisinger et al, 1982;Berridge et al, 1984;Prakash and Norgren, 1991). The central nucleus of the amygdala (CeA) in the forebrain is the most important center for the integration of gustatory and visceral signals (McDonald, 1998) and a lesion to CeA has been proved to influence the sodium appetite of animals (Galaverna et al, 1992Seeley et al, 1993;Zardetto-Smith et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

Inhibitory effect of activation of GABAA receptor in the central nucleus of amygdala on the sodium intake in the sodium-depleted rat

Wang

Yang

et al. 2012

Neuroscience

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Role of sodium concentration of the cerebrospinal fluid in the salt appetite of sheep

Cited by 38 publications

References 0 publications

Water and salt intake of wild rabbits (Oryctolagus cuniculus (L)) following dipsogenic stimuli.

Water and salt intake of wild rabbits (Oryctolagus cuniculus (L)) following dipsogenic stimuli.

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

Inhibitory effect of activation of GABAA receptor in the central nucleus of amygdala on the sodium intake in the sodium-depleted rat

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