Inhibitory effects of estrogen on stimulated salt appetite in rats.

Adult male rats consumed 50–250% more 0.5 M NaCl solution than females did during a 7-hr drinking test when robust salt appetite was elicited by dietary sodium deprivation for 8 days, daily injections of deoxycorticosterone, or adrenalectomy followed by 2 days of sodium deprivation. In contrast, male rats drank much less saline after systemic treatment with the natriuretic agent furosemide, adrenalectomy followed by 1 day of sodium deprivation, or subcutaneous/ly (sc) treatment with colloid solution after 2 days of sodium deprivation, and female rats drank comparably small volumes. Conversely, 30-day-old prepubescent male and female rats showed equally robust salt appetites after 8 days of sodium deprivation. These and other findings support an inhibitory role of estrogen on salt appetite in rats, which appears to occur only when the appetite is especially pronounced. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Sodium depletion enhances salt palatability in rats.

Stereotyped fixed action patterns (FAPs) elicited in rats by oral infusions of taste solutions can be classified as either ingestive or aversive. They reflect the palatability of the taste and can be modified by learning and by the physiological state of the animal. The present 2 experiments, with 5 male Sprague-Dawley rats, demonstrated that when the physiological state of the S was altered by sodium depletion, the pattern of FAPs elicited by oral infusions of 0.5 M NaCl shifted from a mixture of ingestive and aversive components (while sodium replete) to exclusively ingestive ones (while sodium deplete). This shift in taste reactivity occurred the 1st time the Ss were made sodium deplete. A similar shift did not accompany infusions of 0.01 M HCl, a taste solution that also elicited mixed ingestive and aversive FAPs. This result suggests that the shift in response to NaCl was not due to a general change in ingestive bias or to a general taste deficit. On the basis of the change in FAPs, it is concluded that the palatability of highly concentrated salt solutions increases in sodium-deplete rats. Such a shift in salt palatability may be instrumental in directing the appetitive behavior of the animal. (33 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Thirst and sodium appetite after colloid treatment in rats.

In 3 experiments with male albino Sprague-Dawley rats, injection of polyethylene glycol (PEG) solution (10–30% solution) produced a progressive sequestration of extracellular fluid at the injection site. PEG-treated Ss showed both thirst and sodium appetite. However, water intake began 1–2 hrs after the injections, whereas consumption of NaCl solution did not start until 3–4 hrs later. Then Ss ingested both fluids alternately until plasma volumes were restored, whereupon saline intake became even more prominent and water was consumed due to induced osmoregulatory needs. These 3 phases were seen regardless of the dose of PEG or the concentration of saline. After maintenance on a sodium-deficient diet for 2–4 days or after bilateral adrenalectomy, Ss increased their intake of saline immediately after PEG treatment. Findings suggest that the delayed onset of sodium appetite after PEG treatment that occurred when Ss were maintained on standard sodium-rich chow resulted from the buffer provided by surplus extracellular fluid in those Ss. They further suggest that sodium appetite may be stimulated by a decreased availability of sodium in the brain. (44 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Thirst and sodium appetite after colloid treatment in rats with septal lesions.

Previous experiments in which angiotensin II (AII) and mineralocorticoids were administered to rats have suggested that these hormones play a natural role in mediating thirst and sodium appetite. This hypothesis was examined by making use of 20 male Sprague-Dawley rats with septal lesions, which have an apparent sensitivity to the central effects of AII, and by studying their behavioral response to sc treatment with 5 ml of a 30% polyethylene glycol solution, which produces hypovolemia and thereby stimulates the secretions of renin and aldosterone. The induced thirst and sodium appetite both were markedly enhanced in the brain-damaged Ss. However, water intake was not increased when the hypovolemia was moderate, and sodium appetite was augmented only when Ss had been sodium deprived, a procedure known to potentiate aldosterone secretion. Findings support suggestions that while AII normally contributes little to thirst, it may help to mediate sodium appetite in rats when aldosterone is abundant. The 2 drives were not elicited uniformly; those Ss that drank the most water after colloid treatment consumed the least saline. While septal lesions may sensitize the rat's brain to the sodium-appetite-eliciting effects of AII as well as to its dipsogenic effects, sodium appetite may emerge only if the induced thirst is not too pronounced. (16 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Thirst and sodium appetite after colloid treatment in rats: Role of the renin-angiotensin-aldosterone system.

Recent experiments indicated that rats usually develop sodium appetite 5 hrs after sc injection of polyethylene glycol (PEG) solution. However, sodium appetite appeared within 30–60 min if the rats had been maintained on sodium-deficient diet instead of Purina chow for 2–4 days previously. Elevated levels of aldosterone paralleled the appearance of NaCl consumption in both circumstances. In the present experiments, with 65 male albino Sprague-Dawley rats, sodium appetite was no longer potentiated by pretreatment maintenance on sodium-deficient diet when the hypersecretion of aldosterone after PEG administration was prevented by prior hypophysectomy. Conversely, sodium appetite was enhanced in PEG-treated Ss when angiotensin II (AII) was produced in unusually large amounts in the brain, owing to the systemic administration of captopril. This latter effect occurred even when drinking water was withheld and plasma sodium concentrations were markedly elevated. These and other findings raise the possibility that the normal secretion of aldosterone in rats after PEG treatment might permit physiological amounts of AII to be effective in stimulating sodium appetite. Such actions would complement the accepted physiological role of the renin-angiotensin-aldosterone system in the maintenance of blood pressure and sodium balance. (45 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Sodium appetite after transection of the chorda tympani nerve in Wistar and Fischer 344 rats.

Acute sodium depletion in rats leads to dramatic increases in intake of hypertonic NaCl solutions, a behavior known as sodium appetite. The importance of signals conveyed by the chorda tympani (ChT) nerve to the expression of sodium appetite is unclear. The effects of bilateral ChT transection were examined on the short- and long-term response to sodium depletion in Wistar and Fischer 344 (F344) rat strains, because Wistar rats normally display a NaCl preference in the absence of need whereas F344 rats avoid NaCl. In both strains, sodium appetite after ChT transection and treatment with the diuretic furosemide was delayed and blunted or eliminated. The results suggest that signals conveyed by the ChT nerve are important in the expression of a sodium appetite. Effects on F344 rats are particularly interesting because ChT transection surgery appears to have opposite effects on NaCl intake depending on whether F344 rats are sodium replete or deplete. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Sodium appetite in lactating rats.

Lactating rats that were given free access to sodium-deficient food, water, and 0.51 M NaCl solution showed no evidence of sodium appetite. The estimated daily loss of 1–2 mEq Na in milk was replaced by basal daily intake of 2–5 ml of saline. Sodium loss in urine was minimal, but milk sodium concentration was unchanged, and pups grew normally. Saline intake was enhanced when lactating rats that had been maintained on standard laboratory chow were injected with 30% polyethylene glycol solution to reduce plasma volume but no more so than when virgin female rats or male rats were similarly colloid-treated. Lactating rats markedly increased their intake of NaCl solution after simply depriving them of dietary sodium for 4 days, whereas male and virgin female rats did not. These findings indicate that pronounced sodium appetite does not invariably accompany lactation in rats, although it can occur whenever such animals become hypovolemic or sodium deficient. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Enhanced sodium appetite in rats with lesions centered on nucleus medianus.

Recent experiments have demonstrated that rats with lesions of the ventral portion of nucleus medianus (VNM) frequently exhibit a chronic and robust hyperdipsia, which occurs only at night. The present study demonstrated that the same brain damage may produce a nocturnal appetite for sodium that is similarly pronounced and persistent. Of 68 male Sprague-Dawley rats with VNM lesions, 33 were observed to drink at least 15 ml of 0.51 M NaCl solution per day, and 11 of them consumed more than 30 ml daily. The basis for this high consumption of saline is uncertain; the brain-damaged Ss had normal sodium concentrations, renin activities, and aldosterone levels in plasma during basal maintenance conditions, and they conserved sodium in urine when maintained on a sodium-deficient diet. Nevertheless, the present results indicate that VNM and/or local fibers of passage may play an important role in the control of sodium appetite, as it does in the control of thirst. (19 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Sex and sodium intake in the rat.

Female rats drink more 3% NaCl solution than do males, both when they need sodium (need-induced sodium intake or sodium appetite) and when they do not (need-free sodium intake). The sexual dimorphism of sodium intake is a secondary sexual characteristic because after castration at 1 day of age, male rats drank 3% NaCl in adulthood in a manner similar to that of females in both the need-free and need-induced state, and females given long-term neonatal testosterone drank low, malelike volumes of 3% NaCl on a daily need-free basis, but their response to sodium depletion was unchanged. This sexual dimorphism of sodium intake seems to be governed by testosterone that has been converted in the brain to estrogen because treatment of Day 1 castrated females with a nonaromatizable androgen, dihydrotestosterone, did not change either their need-free or their need-induced 3% NaCl intake. Castration in adulthood of male and female rats did not change their sodium consumption… (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Sodium appetite in adrenalectomized rats following dietary sodium deprivation.

Experimented with operated, sham-operated, and comparison male Sprague-Dawley rats (N = 74). Adrenalectomized (Adrex) rats adjusted well during adrenal insufficiency when saline solutions were available. Despite continuous uncontrolled losses of relatively large amounts of sodium in their urine, they managed to maintain body fluids at approximately normal levels by replacing crucial sodium losses, if only temporarily, through frequent intakes of saline. It is concluded that the threshold for sodium appetite in Adrex rats is associated with relatively small sodium deficits, and roughly similar deficits also are effective in stimulating sodium appetite in intact Ss. When more pronounced losses result from maintenance on a sodium-free diet, Adrex Ss rapidly drink more than enough saline to replace their deficits. Thus, it seems evident that mineralocorticoids need not have a vital role in either the initial salt-drinking response of intact Ss to minor sodium deficits or their overcompensation for moderate sodium deficits. (32 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Salt seeking by food selection in adrenalectomized rats.

Investigated the generality of salt-seeking behavior in 2 experiments with 12 sham-operated and 9 adrenalectomized male albino Dublin strain rats. Under diets which differed in salt content, the adrenalectomized Ss selected salty over plain food. Where the salt concentration was 3% or greater, the adrenalectomized Ss maintained body weight and showed no adverse symptoms. Contrary to previous theories, results demonstrate that when salt is available in food, rats do seek out and can consume NaCl in sufficient quantities to maintain sodium levels. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effect of potassium depletion on mineral appetite in the rat.

Studied potassium appetite in normal female Sprague-Dawley rats and in rats in which the total body potassium had been reduced by 15-20%. Potassium depletion resulted in increased ingestion of solutions of NaCl, KCl, CaCl2, and quinine sulphate in concentrations that were unacceptable to normal Ss. The amount of potassium ingested was related to the degree of potassium depletion and repletion was usually completed within 24 hr. when potassium was offered. Potassium-depleted Ss also drank large quantities of aversive concentrations of sodium chloride. This was preferred to potassium chloride and its ingestion appeared to be unrelated to need. The appetite state was reversed by prior intragastric repletion with potassium but not with sodium salts. (19 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Behavior of sodium-deficient rats: The search for a salty taste.

Tested whether 188 Na-deficient rats would search for the taste of Na or the taste of salt. Ss were subjected to various conditions of food and water deprivation before being given a choice between solutions of varying saltiness. Na-deficient Ss displayed an appetite for solutions that humans judged as salty-tasting whether or not the solutions contained sodium salts. When offered a choice between a pair of sodium salts, Ss generally preferred the more salty-tasting solution. They tended to do the same for a pair of nonsodium salts and for a pair of sodium and nonsodium salts. Results show that human psychophysical judgments of saltiness are a good predictor of the choices that rats will make when Na-deficient. (22 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Changes of blood pressure responsiveness in rats exposed in utero and perinatally to a high-salt environment

We tested the hypothesis that the pressor responses to angiotensin II could be influenced by an early salt exposure. Twenty-five adult female rats were pseudorandomly divided in two groups. Twelve animals underwent a partial ligature of their abdominal aorta (PAL). Once polydipsia and sodium appetite developed, these rats were mated. The other group (13 rats) was sham-operated (Sham) and mated. Throughout pregnancy and lactation, water and 2.7% NaCl solution intakes differed between the two groups of mother rats. PAL offspring (PAL-O; n = 14), and Sham-operated offspring (Sh-O; n = 10), were maintained on a solid diet containing 1% NaCl, tap water and a 2.7% NaCl solution. At 90 days of age, pressor responsiveness to intravenous angiotensin II (50, 100 and 200 ng) was assessed in anesthetized rats. The pressor responses to 50 and 200 ng angiotensin II were significantly greater in PAL-O rats than in Sh-O rats. These results support the hypothesis of a modulation of cardiovascular responsiveness or its underlying mechanisms by an early high salt environment.     

Relationship between absolute body-fluid deficits and fluid intake in the rat.

In 5 experiments acute absolute body-fluid deficits were induced in a total of 36 male albino Sprague-Dawley rats by injection of the diuretic drug furosemide, which caused up to 20% reduction of extracellular fluid volume and up to 2% reduction of intracellular fluid volume. Water and .3 M NaCl were subsequently made available to allow the Ss to replace their body fluids by drinking. The Ss increased their intake of both fluids, but replaced less than half of the total deficit, thereby tolerating larger and larger voluntary body-fluid deficits as the size of the diuretic fluid loss increased. Plasma measures showed that the Ss sustained hypovolemia after drinking, while intracellular fluid volume was apparently restored. Fluid-depleted Ss drank normally in response to intracellular dehydration induced by a sodium chloride load. Results demonstrate that incomplete restoration of body-fluid balance after body-fluid depletion is due to a failure to drink in response to extracellular dehydration. (28 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Induction of an appetite for sodium in rats that show no spontaneous preference for sodium chloride solution—The Fischer 344 strain.

Fischer 344 rats show no spontaneous preference for isotonic NaCl solution. These experiments indicate, however, that a strong appetite for this solution may be induced by various methods, including adrenalectomy, administration of a mineralocorticoid hormone, acute depletion of sodium, and treatment with inhibitors of the angiotensin I converting enzyme. These treatments were also shown to produce the expected changes in the renin-angiotensin-aldosterone system, which thus appears to be involved in the induction of an appetite for NaCl solution in this strain of rat. The intakes of NaCl induced in the Fischer 344 rats by these experimental paradigms are less than those that have been reported in either Sprague-Dawley or Wistar strains in similar paradigms. In the case of sodium depletion, the intake of NaCl solution by Fischer 344 rats appears to be more closely related to the deficit than in the other 2 strains. The Fischer 344 strain of rats may be a particularly good model for studies of need-related sodium appetite. (PsycINFO Database Record (c) 2011 APA, all rights reserved)     

Dependence of adrenalectomy-induced sodium appetite on the action of angiotensin II in the brain of the rat.

Adrenalectomized rats express a robust sodium appetite that is accompanied by high levels of blood-borne angiotensin II and is caused by angiotensin II of cerebral origin. Blood-borne angiotensin II is elevated in rats consuming NaCl after adrenalectomy, and plasma angiotensin II concentrations are increased further when the animals cannot drink a NaCl solution. These phenomena are the result of the pathological removal of aldosterone, because replacement therapy returned both sodium intake and plasma angiotensin II concentrations to preadrenalectomy levels. The adrenalectomized rat's appetite for sodium is completely suppressed by interference with the central, but not the peripheral, action of angiotensin II. These data demonstrate that the mechanism of the sodium appetite of the adrenalectomized rat is a pathological instance of the angiotensin/aldosterone synergy that governs the sodium appetite of the adrenal-intact, sodium-depleted rat. Because aldosterone has been removed, angiotensin acts alone to produce the appetite. Furthermore, the data show that it is angiotensin II of central origin that is important for sodium appetite expression. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Chronic immobilization stress reduces sodium intake and renal excretion in rats

The influence of chronic exposure to immobilization (IMO) on sodium appetite as well as sodium and potassium renal excretion in adult male Wistar rats was studied. The animals were individually housed and all variables under observation were measured in metabolic cages the first, seventh, and thirteenth days once the experiment had started. Half of the rats had access to water, and the remainder of the rats had access to both water and saline solution (1.5% NaCl). IMO reduced the intake of saline solution. Renal water, sodium, and potassium excretion in those IMO rats having access to saline were lower than in control rats. The effects of IMO were very similar during all observation days; therefore no evidence of adaptation to repeated stress was found. The present data indicate the following: (i) IMO stress reduced sodium appetite, probably as a secondary effect to the deficit in sodium renal excretion; (ii) IMO caused antidiuresis and antikaliuresis, only in those rats taking saline solution; (iii) no adaptation to repeated IMO stress was found in any of the tested variables. The reduction of sodium appetite observed in stressed rats might be a homeostatic mechanism to maintain sodium balance after impairment of renal sodium excretion caused by stress.     

Interaction of hydration and subfornical organ lesions in sodium-depletion induced salt appetite.

The authors tested whether the level of hydration after furosemide diuresis and 22 hrs of sodium depletion affects the amount of water or 0.3 M NaCl solution consumed by rats with intact brains or with lesions of the subfornical organ (SFO). Rats received 2 (underhydrated) or 10 (euhydrated) ml/kg water by gavage as the only fluid input 2, 4, and 20 hrs after 10 mg/kg furosemide. These hydration treatments had little or no effect on the amount of saline consumed in 2 hrs by intact rats. SFO lesions reduced water intake regardless of hydration condition. Euhydrated, SFO-lesioned rats drank a normal amount of saline, but underhydrated, lesioned rats drank less saline than any other group. Thus, euhydration may facilitate salt appetite in SFO-lesioned rats, and the deficits in salt appetite noted in SFO-lesioned rats may result from deficits in water ingestion rather than from a destruction of angiotensin II receptor sites that directly provoke salt appetite. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Sodium homeostasis in chronic decerebrate rats.

Two experiments examined physiological and behavioral concomitants of sodium need in supracollicularly transected and pair-fed intact male Sprague-Dawley rats. Chronic decerebrate Ss, like intact Ss, reduced their urine sodium output when placed on a sodium-deficient diet. Similarly, 24 hrs after sodium loading, decerebrate and intact Ss excreted comparable levels of the excess sodium. In the 2 hrs immediately following loading, decerebrate Ss excreted less sodium. In contrast, behavioral aspects of sodium homeostasis were completely absent in chronic decerebrate Ss. In separate experiments, intraoral intake and taste-reactivity responses elicited by intraoral infusions of NaCl were measured during sodium-replete and sodium-deficient conditions. In response to oral infusions of NaCl, intact Ss consumed significantly more and produced greater numbers of ingestive taste-reactivity responses when they were sodium deficient than when they were sodium replete. The same sodium-depletion treatments in chronic decerebrate Ss, however, altered neither the intraoral intake of NaCl nor the frequency of NaCl-elicited ingestive taste-reactivity responses. Results suggest that the behavioral compensatory responses that follow changes in the internal sodium state depend on forebrain mechanisms. (53 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)