Appetite For NaCl Research Articles

Parabrachial lesions in rats disrupt sodium appetite induced by furosemide but not by calcium deprivation

An appetite for CaCl2 and NaCl occurs in young rats after they are fed a diet lacking Ca or Na, respectively. Bilateral lesions of the parabrachial nuclei (PBN) disrupt normal taste aversion learning and essentially eliminate the expression of sodium appetite. Here we tested whether similar lesions of the PBN would disrupt the calcium-deprivation-induced appetite for CaCl2 or NaCl. Controls and rats with PBN lesions failed to exhibit a calcium-deprivation-induced appetite for CaCl2. Nevertheless, both groups did exhibit a significant calcium-deprivation-induced appetite for 0.5M NaCl. Thus, while damage to the second central gustatory relay in the PBN disrupts the appetite for 0.5M NaCl induced by furosemide, deoxycorticosterone acetate, and polyethylene glycol, the sodium appetite induced by dietary CaCl2 depletion remains intact.

Calcium-deprived rats sham-drink CaCl2and NaCl

Calcium-deprived rats are often thought to increase their calcium intake as a result of learning, but recent studies indicate that there is also an unlearned component to the appetite. They also ingest large amounts of some non-calcium minerals, including sodium. We examined the contribution of post-ingestive feedback to drinking using calcium-deprived and replete rats that could sham-drink CaCl2and NaCl. Rats fitted with gastric cannulae in order to allow ingested fluids to drain freely drank 0·3M NaCl in six 1-h sessions with their cannulae open (sham), followed by two sessions with their cannulae closed. Their intake of 0·03M CaCl2was then measured in a similar series of tests (six with cannula open followed by two with it closed). Ingestion of both NaCl and CaCl2was significantly greater in calcium-deprived than in replete subjects under both open and closed conditions. These differences reached significance within 15min after the onset of drinking during the first test with NaCl, and within 5min in subsequent tests. The differences in CaCl2intake generally reached significance within 5min, including during the first test. Because there was minimal opportunity for post-ingestive NaCl or CaCl2to mediate learning, the results provide additional support that the appetite for CaCl2and NaCl in calcium-deprived rats can be driven solely by orosensory factors.

Adrenalectomy enhances the anorectic effect of dexfenfluramine: Relation to mineralocorticoids and salt appetite

A previous observation that adrenalectomized (ADX) rats were more anorectic and lost more weight than intact controls when treated with the serotonergic agent, d, l-fenfluramine, was confirmed using a high dose of the more selective d-enantiomer, dexfenfluramine (DFEN). However, ADX rats were not more anorectic than intact controls to a lower dose of DFEN. The extreme weight loss at high doses was accompanied by a loss of appetite for NaCl solution. The rapid deterioration of these animals may have been due to excessive loss of sodium ions and extracellular fluid volume, although this was not assessed directly. This interpretation was supported in a second study in which treatment of ADX rats with a selective mineralocorticoid, which eliminates both the need and appetite for NaCl, normalized weight loss during DFEN treatment. These data do not support the idea of an interactive role of glucocorticoids and brain serotonin in anorexia. The density of serotonin uptake sites in frontal cortex was reduced by DFEN in a dose-dependent manner, but did not differ between ADX and intact control groups.

Sodium appetite in rats after prolonged dietary sodium deprivation: a sexually dimorphic phenomenon

Little sodium appetite is observed when rats are deprived of dietary sodium for several days, presumably because aldosterone secretion minimizes renal sodium losses. However, the present studies indicate that when sodium deprivation is extended to 8 days, a spontaneous sodium appetite results that far exceeds urinary sodium losses during the deprivation period; indeed, adult male rats drank as much 0.5 M NaCl solution as rats ever have been reported to drink rapidly. In contrast, female rats drank much less saline after 8 days of sodium deprivation. Because of this sexual dimorphism in sodium appetite, we also studied NaCl intake in gonadectomized rats after 8 days of sodium deprivation. Both male and female gonadectomized rats drank comparable amounts of saline as intact male rats, but they consumed much less when treated with physiological amounts of estrogen during the sodium-deprivation period. These results indicate that a robust appetite for NaCl can be produced in rats by prolonged sodium deprivation and that estrogen can blunt the induced sodium appetite.

Sodium appetite: Species and strain differences and role of renin-angiotensin-aldosterone system

The characteristics of the appetite for NaCl in humans differ in some aspects from those in other species. The mechanisms of appetite for NaCl have been studied in detail in two species, rats and sheep. We review the treatments known to induce an appetite for NaCl in rats, with special reference to differences among strains in their spontaneous preference for NaCl solution. The current view of the mechanism is critically appraised, with particular emphasis on the role of angiotensin II, mineralocorticoids, cerebroventricular sodium transport, and the relation between preference for NaCl and the concentration of sodium in saliva. The appetite for NaCl in rodents other than rats is considered next, and reveals that mice, hamsters and gerbils are reluctant to ingest NaCl either spontaneously or after treatment with several of the natriorexigenic stimuli that are effective in rats. The characteristics of the appetite for NaCl in non-rodent species, including sheep, rabbit, dog, and non-human primates, are then described. We discuss some of the possible differences in mechanism that might account for this behavioral diversity among species.

Regulation of intakes of water and NaCl solutions in Fischer 344 rats: Contrasts and comparisons between strains

We present an overview of the differences in intakes of both water and NaCl between different strains of rat, with emphasis on Fischer 344 (F344) and Sprague-Dawley (SD) strains. Relative to SD, rats of the F344 strain show less spontaneous or secondary drinking both with food present and during food deprivation. The water intake of rats of the F344 strain is strongly inhibited when water is added to their food, but rats of the SD strain show less inhibition and consume excessive amounts of fluid. In studies of primary drinking, induced by treatment with various dipsogens, rats of the F344 strain consumed water in amounts that were generally comparable to those expected from rats of the SD strain, with the exception of reduced intakes in response to either polyethylene glycol-induced hypovolemia or treatment with isoproterenol. The hematocrit ratio, resting plasma renin activity and directly-measured plasma protein concentrations were similar between F344 and SD strains. We also review findings that rats of the F344 strain show no spontaneous preference for dilute NaCl solutions, and show that both a strong preference and a low preference threshold are induced by chronic treatment with ramipril. Other manipulations that induce an appetite for NaCl in the F344 strain are summarized.

Re-examination of the effect of either a lateral or third ventricular cannula on captopril-induced salt appetite in rats

In Study A, rats were implanted with a cannula aimed at either the lateral (LV) or ventral third (V3V) brain ventricles 1 week prior to starting a chronic oral regimen of captopril. The presence of neither cannula significantly impaired the emergence of captopril-induced appetite for NaCl solution. In Study B, V3V cannulae were implanted in rats after a captopril-induced appetite for NaCl was established. The surgery produced a 1–2 day attenuation of NaCl intake, but this was no greater than that observed in a sham-operated group that received no cannula. These results do not support those of others who suggest that captopril (and, by inference, other agents) can leak across a damaged blood-brain barrier for at least 2 weeks after placement of a cannula. Possible reasons for the differences in results are addressed.

Role of renin-angiotensin-aldosterone system in NaCl appetite of rats.

A variety of experimental paradigms is now known to induce an appetite for NaCl solutions in rats. These include 1) bilateral adrenalectomy; 2) hypothyroidism; 3) salivariectomy; and 4) administration of hydrochlorothiazide, metyrapone, estrogen, methylxanthines, captopril, propranolol, large doses of deoxycorticosterone acetate, and intraperitoneal isotonic glucose or subcutaneous polyethylene glycol. A point of commonality among these is that a reduction in preference threshold accompanies the appetite for NaCl in all cases thus far tested. An additional point is the fact that each paradigm inducing a salt appetite, except salivariectomy, can be linked to an effect on the renin-angiotensin-aldosterone system. The level of angiotensin II in the brain may play a role in the induction of a salt appetite in the rat. It is clear, however, that modest doses of mineralocorticoid hormones, given in conjunction with the stimulus producing the salt appetite (e.g., adrenalectomy, thyroidectomy, or treatment with captopril), reduces NaCl intake to control level. Although this effect can be partially explained in most cases by the consequent reduction in angiotensin II production, the salt appetite that occurs when mineralocorticoid concentration in blood is high and angiotensin II concentration is low, or when both are low, requires another explanation. This may be related to the effect of mineralocorticoid hormones on salivary sodium concentration. The role of the concentration of sodium in saliva on intake of NaCl solution provides an alternative explanation for the induction of a salt appetite in rats and merits additional study.

Effects of dorsal, mediobasal and laterobasal septal lesions in the rat: Water and sodium chloride intake

Under the conditions of a free choice between water and saline and with solid standard food ab lib., male rats with a lesion localized in the septum display a higher daily intake of NaCl than controls; the amount taken up represents the total NaCl taken in both saline and solid food. Rats with septal lesions have a higher total intake of liquids depending on experimental conditions and, in some cases, on the localization of the lesion. The consumption of water remains the same while the amount of the NaCl solution consumed increases. The molar concentration of the total NaCl consumption taken up with both the solution and the solid food, referred to the total fluid intake, is the same in control rats and in operated animals under all experimental conditions. The consumption of solid food by rats with septal lesions and, hence, the consumption of NaCl from the pellets, was increased depending on experimental conditions. The increase was observed in rats during the resting period, during the first application of fighting tests, and, in rats having the lesion in the laterobasal septal region, also during a repeated fighting period. The increased consumption of NaCl in rats with septal lesions reflects the fact that they drink more saline as compared with controls (by 86%). The increase in NaCl consumption due to solid food is only 24% as compared to controls. Mutual differences between septal rats with different localization of the lesion are only quantitative and depend on the conditions under which the animals are kept. Rats with lesion in the dorsal and mediobasal regions have a higher saline intake both when resting and exposed to a stimulation; the type of stimulation is of no importance in these animals. Rats with laterobasal lesion have a higher saline intake in the first stimulation period only. A hypothesis is discussed concerning the effect of septum on the appetite for NaCl.

Investigations into specific appetites for sodium and thiamine in domestic fowls

It was not possible to demonstrate a specific appetite for NaCl in sodium-deprived chickens, regardless of whether the deprivation was induced by feeding a deficient diet or by producing a functional deficiency by the subcutaneous injection of formalin. Such birds exhibited a preference neither for NaCl-supplemented diets nor for 0.7% saline when tested in two-choice situations. Normal chickens were indifferent to 0.7% saline when tested by the method of single stimuli, but under simultaneous-choice conditions showed a strong aversion to it, which intensified as time passed; this was explained in terms of aversive feedback. Thiamine deficiency was induced in chickens by feeding a metabolic antagonist, and a well-marked specific appetite for this vitamin could be demonstrated in these deficient birds.

Increased Sodium Chloride Appetite during Pregnancy in the Rat

It was the purpose of this study to determine whether an increased appetite for NaCl could prevent the previously observed deleterious effects of Na restriction during pregnancy in the rat. Both NaCl solution and distilled water were made available to nonpregnant and pregnant rats given adequate or restricted levels of dietary Na intake. Although no differences appeared in the total fluid consumption by rats given the two levels of Na intake, the proportion of fluid intake from NaCl solution and distilled water was significantly different and dependent upon dietary Na level. The biochemical, histological, and histochemical effects of restricted Na intake during pregnancy previously reported by this laboratory did not appear in animals with access to NaCl solution. The data clearly indicate an increased appetite for NaCl during pregnancy which leads to increased intake. If this is permitted to operate, extraordinary stress on the renin-aldosterone mechanism of Na conservation is prevented.

Specific appetite for NaCl without postingestional repletion.

Specific appetite for NaCl without postingestional repletion.

Specificity of the sodium chloride appetite of adrenalectomized rats; substitution of lithium chloride for sodium chloride.

A cafeteria or choice experiment was performed to determine the specificity of the NaCl appetite of adrenalectomized rats. In this experiment fluid intakes of male adrenalectomized rats were compared with those of male controls. All animals were allowed to choose freely between distilled water and a salt solution as drinking fluids. Nine different salt solutions were used with at least three separate concentrations of each salt being given. The salts used were: NaCl, LiCl, KCl, CaCl2, Na2SO4, Na citrate, Na oxalate, NaI and NaHCO3. Adrenalectomized rats showed a specific appetite for NaCl and gained weight only when this salt was given. Though greater volumes of Na2SO4, NaHCO3 and and Na citrate solutions were ingested than water, adrenalectomized rats lost weight on all of these. Normal rats failed to manifest an appetite for any of the salts offered. Particular attention was given to LiCl since this salt has been reported by others to stimulate chemoreceptors of the tongue of the anesthetized rat to produce electrical responses which are similar in amplitude to those initiated by the same concentration of NaCl. Both normal and adrenalectomized rats were given choice between NaCl solutions and water and later, between LiCl solutions and water. In equimolar concentrations, LiCl could not be substituted for NaCl; these two salts did not appear to ‘taste’ the same to either unanesthetized normal or adrenalectomized rats. Other experiments revealed that it was not possible to mask the ‘taste’ of LiCl in solution by mixing varying amounts of NaCl with it. However, a possibility exists that LiCl and NaCl taste the same to adrenalectomized rats and that LiCl is rejected because its toxic effects are manifested when small amounts are ingested.