Preoperative sodium experience and hypothalamic lesions in rats.

When a sodium deficit is induced in rats without lesions, they increase their saline intake regardless of prior experience. By contrast, the present experiment with 60 Sprague-Dawley rats found that Ss with lateral hypothalamic lesions increased their saline intake only when they had had preoperative experience ingesting saline in response to a sodium deficit. Ss were given natriuretic and mineralocorticoid treatments to induce sodium appetite. The role of preoperative experience in neural function is discussed. (32 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)     

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)     

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)     

Preoperative latent place learning preserves salt appetite following damage to the central gustatory system.

Points out that rats given the experience of tasting saline before receiving lesions in the region of the thalamic taste relay are protected from the usual lesion-induced deficits in salt appetite. In the present study with 48 male Sprague-Dawley rats, the location of the saline during postoperative testing was varied from the location during preoperative training for some Ss and kept the same for others. A clear protective effect was evident when the preoperative and postoperative locations were the same but not when they were different. This protective effect may be due to place learning because it is known that rats can remember tasting saline in a particular place and then return there when in a state of sodium need. (30 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of basolateral amygdala lesions on neophobia, learned taste aversions, and sodium appetite in rats.

Reports results of 8 experiments with a total of 327 male Sprague-Dawley rats. Lesions to the basolateral amygdala produced permanent impairment in Ss' ability to learn a taste aversion. When lesions were administered after Ss had already learned an aversion, there was complete loss of the aversion. Ss with amygdala lesions also had a diminished neophobic response when presented with a novel solution and showed a more generalized aversion to water after a sucrose-sickness trial. Whether a solution was novel or familiar affected the learning of an aversion for controls more than it did for Ss with amygdala lesions. Ss with amygdala damage also showed less sodium appetite than normals in response to desoxycorticosterone acetate injections. These results indicate that rats with amygdala lesions have deficits in recognizing the significance of stimuli. (49 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Escape from deficits in sodium intake after thalamic lesions as a function of preoperative experience.

Saline and water intakes in response to treatments with a natriuretic agent and a mineralocorticoid were studied in intact Sprague-Dawley male rats and in rats with lesions centered in the taste relay of the thalamus. Intact Ss responded to the treatments by increasing both saline and water intake. Ss with thalamic lesions that had never drunk saline prior to induction of the lesions generally did not increase their saline intake in response to the treatments but showed normal increases in water intake. In contrast, Ss with thalamic lesions that had drunk saline prior to induction of the lesions showed normal increases in both saline and water intake. Preoperative experience of sodium need did not protect Ss against the lesion-induced deficit. (22 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Mineralocorticoid receptor antagonism prevents hedonic deficits induced by a chronic sodium appetite.

Our laboratory has reported that manipulations that provoke a robust sodium appetite (e.g., sodium depletion, deoxycorticosterone acetate) decrease lateral hypothalamic self-stimulation (LHSS) reward if rats are denied access to hypertonic saline solutions. The following studies investigated the interaction between chronic sodium appetite and the renin-angiotensin-aldosterone system on LHSS reward. In Experiment 1, animals treated with the diuretic furosemide (20 mg/kg) when denied access to saline exhibited an increase in the current required to produce 50% of the maximum LHSS response rate (ECu50) 48 hr after extracellular volume depletion. Furosemide-depleted rats that were allowed to drink 0.3 M saline after depletion, or that were treated with the selective mineralocorticoid receptor (MR) antagonist spironolactone, which significantly reduced sodium appetite, did not show ECu50 changes. In Experiment 2 chronic intracerebroventricular administration of the selective MR antagonist RU 28318 (10 μg/μl/hr) prevented decreases in the ECu50 induced by deoxycorticosterone acetate-no salt treatment. We conclude that an unresolved sodium appetite will reduce responding for rewards and that experimental manipulations that reduce sodium appetite (e.g., access to saline or blockade of MR) decrease hedonic deficits. (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)     

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)     

Salt appetite and lesions of the ventral part of the ventral median preoptic nucleus.

Angiotensin receptors in the most ventral part of the ventral median preoptic nucleus (VVMnPO) or organum vasculosum laminae terminalis appear to be important for salt appetite to angiotensin in rats. If so, then small lesions of this region should reduce salt appetite that is dependent on angiotensin. In separate experiments, the lesion greatly reduced salt appetite after treatments with chronic oral captopril or sodium depletion. On the other hand, the VVMnPO lesion actually enhanced salt appetite to deoxycorticosterone acetate. The lesion did not affect water intake to water deprivation, combined food-water deprivation, isoproterenol, or hypertonic saline, and basal plasma osmolality and sodium values were normal. These experiments suggest that VVMnPO lesions selectively affect angiotensin-induced salt appetite without producing the gross hydrational deficits that occur with larger lesions of the ventral forebrain. (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)     

Canine babesiosis in South Africa: more than one disease. Does this serve as a model for falciparum malaria?

The present study was carried out to determine whether the increased salt intake induce by increased specific sodium appetite in pregnant rats modifies water-salt homeostasis throughout pregnancy. Two groups of pregnant rats were used, one fed ad libitum with a normal sodium (NS) diet consisting of standard rat chow and distilled water, and the other fed with a high-sodium (HS) diet with free access to chow, distilled water plus saline solution (1.5% NaCl). Virgin rats in dioestrus were also studied as non-pregnant controls. Pregnant animals were studied on days 4, 9, 14, 20 and 21 of gestation at which time body weight, water and saline intake, sodium excretion, plasma atrial natriuretic peptide (ANP) and arginine vasopressin (AVP) concentrations, as well as plasma osmolality were determined. Data showed that water intake was higher in the NS group, but total fluid intake (water plus saline) was higher in the HS group throughout pregnancy. Dietary sodium intake was the same for both groups but total sodium intake (chow plus saline) was 60-98% higher in the HS rats. Pregnant HS rats excreted more fluid (35-50%) and sodium (up to 100%) compared with NS rats, indicating that the animals could change their renal excretion in response to a 2.5-fold higher dietary sodium intake compared with the control level. Salt satiety during pregnancy did not modify plasma ANP concentration. In both groups of pregnant rats ANP levels increased 3-fold on day 14 without significant alteration in sodium excretion, suggesting that the natriuretic action of ANP is attenuated at least after the second week of pregnancy. High sodium intake did not change plasma AVP concentration or osmolality and both groups showed the same gradual decrease in plasma osmolality (approximately 8 mosmol kg-1) at the end of pregnancy that was not accompanied by decreased plasma AVP concentration. The present data show that rats maintain the special homeostatic equilibrium that occurs in normal pregnancy even when they are allowed to increase sodium intake to satisfy their salt appetite during this period of the reproductive cycle.     

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)     

Refined salt appetite methodology for rats demonstrated by assessing sex differences.

Describes a refined method for inducing and measuring salt appetite for studying behavioral and neurological functions. The efficiency and reliability of the procedures were demonstrated by parametric studies comparing the appetite behaviors of male and female rats. The method for inducing salt appetite coupled 2 days of dietary sodium deprivation with a brief diuretic treatment. The measurement procedure involved a 2-hr period of access to one of several NaCl solutions differing in palatability or concentration. The induction procedure allowed precise control of drive levels, and the measurement procedure yielded highly reliable results as a function of the properties of the incentives. 32 female mongrel rats consistently ingested about twice as much NaCl solution as did 32 male Ss, regardless of the palatability of the solution or of body sodium levels. At the same time, female Ss lost less sodium in urine following diuretic treatment. (16 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Water and NaCl intake after furosemide treatment in sheep (Ovis aires).

Iv infusions of the natriuretic drug furosemide in sheep led to the excretion of large quantities of hypotonic urine. Ss consumed more water than was needed simply to restore osmotic equilibrium. The stimulus for the additional intake was presumably hypovolemia resulting from the loss of sodium in urine. Despite the natriuresis, in only 2 of the 15 experiments did sheep drink significant amounts of .5 M NaCl solution during the first 10 hrs after the onset of furosemide treatment, and hemoconcentration and arterial hypotension were evident during this time. By 24 hrs, however, the saline consumption in all but 3 experiments had increased and compensated adequately (together with the water intakes) for the furosemide-induced loss of sodium-rich fluid in urine. Results provide evidence that following acute hypovolemia in sheep, as in rats, the onset of sodium appetite is delayed relative to the appearance of thirst. (29 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 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)     

Angiotensin and salt appetite: Physiological amounts of angiotensin given peripherally increase salt appetite in the rat.

In 2 experiments, adrenalectomized male Sprague-Dawley rats were maintained ad lib on distilled water, 3% saline, and sodium-free food. In Exp I, 45 Ss were given desoxycorticosterone acetate (DOCA [.1–2 mg/kg/day, intramuscularly]) for 5 days to determine the dose of DOCA that would produce the lowest voluntary saline intake, and 800 μg/kg/day was found to produce the nadir in saline intake. In Exp II, 40 Ss were placed ad lib on distilled water, saline, and sodium-free food as described above, maintained on 800 μg/kg/day DOCA, and infused with 4, 25, or 100 μg/kg/day angiotensin II (AII) or 0.9% saline. The 3 AII groups showed significant percentage changes in their saline intake above pre-AII levels; the saline control group showed no change in saline intake from pre-AII level. Results demonstrate the production of salt appetite in rats by peripheral administration of physiological doses of AII. (25 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Abdominal vagotomy inhibits osmotically induced drinking in the rat.

Results of a study with 35 male Sprague-Dawley rats show that after complete bilateral transection of the abdominal vagus (Vgx-C9), with the hepatic branch left intact, Ss drank later and less than normal after cellular dehydration induced by hypertonic saline. When access to water was delayed for 1 hr after cellular dehydration, Vgx-C Ss initiated drinking quickly with normal latency, but (a) a gastric water preload was a more effective stimulus for drinking suppression in Vgx-C than in normal Ss; (b) gastric emptying of a water or phenol red solution preload was more rapid in Vgx-C than in normal Ss; and (c) when gastric emptying dysfunction in Vgx-C Ss was removed by having Ss sham drink, Vgx-C and normal Ss sham drank equivalent amounts of water. Thus, disordered preabsorptive satiety caused by abnormally rapid gastric emptying of water was a factor in the decreased drinking of Vgx-C rats after cellular dehydration. Disordered satiety for ingested water could not, however, account for the abnormal latency to initiate drinking after cellular dehydration in Vgx-C rats. (29 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)