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PubMed1980

Increased sodium appetite in the rat induced by intracranial administration of components of the renin-angiotensin system.

1. Intracranial injections of components of the renin-angiotensin system in rats in normal water and Na balance caused an immediate thirst followed by a progressive increase in Na appetite during a test session which lasted 18 h. The effect on water and Na intake was dose-dependent. 2. Long-term (7 day) infusions of angiotensin II into the third cerebral ventricle at rates of 1 or 10 pmol h-1 produced large and sustained increases in intake of water and 2 . 7% NaCl. Intakes sometimes exceeded 100 ml 2 . 7% NaCl per day but quickly fell to normal when the infusion was stopped. 3. Intracranial injection or infusion of carbachol caused a transient increase in water intake but had no effect on the intake of NaCl. 4. The Na appetite induced by intracranial injection of angiotensin was specific for Na since rats offered a choice of water and equimolar concentrations of NaCl and KCl took only water and NaCl. This resembles the pattern seen in Na-depleted rats. 5. Increased Na appetite was not secondary to increased water intake since it occurred when only 2 . 7% NaCl was available to drink. 6. Increased Na appetite was not secondary to natriuresis since, first, the angiotensin-stimulated rats went into positive Na balance, secondly, intracranial renin did not cause increased Na excretion in Na-loaded rats and thirdly, anureic rats showed a significant Na appetite in response to renin. 7. These results suggest that angiotensin in the brain may play a role in the development of Na appetite.

Angiotensin II↗
PubMed1982

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

The role of sodium concentration of the cerebrospinal fluid (CSF[Na]) in the initiation and/or satiation of Na appetite of Na-deplete or Na-replete sheep was investigated. Slow infusion (1 ml/h) into a lateral brain ventricle of an artificial sheep CSF solution was begun 0-60 min prior to and continued until the end of the Na access period (30-120 min). In Na-deficient sheep, increasing CSF[Na] caused a decrease in Na intake. In both Na-deficient and Na-replete sheep, decreasing CSF[Na] caused an increase in Na intake. The appetite was observed within 25 min of beginning infusion, which represents the most rapid induction of Na appetite yet observed. In Na-replete sheep, the appetite induced by decreasing CSF[Na] was predominantly for Na-containing solutions. A decrease in CSF[Na] of only 4-6 mmol/l was sufficient to induce Na appetite. The results derived by use of different Na, saccharide, or urea containing artificial CSF solutions suggest that there are sensors within the neuropil that respond to change of [Na] and influence salt appetite. They can be accessed by inducing change in [Na] of cerebroventricular CSF.

Animals↗
PubMed1991

Selective effects of sodium and chloride depletion on salt appetite in rats.

Findings from hypertension research indicate that dietary sodium chloride (NaCl), Na+, and Cl- independently influence blood pressure, electrolyte metabolism, and hormone secretion. In this context, we examined the effects of NaCl, Na+, and Cl- depletion, respectively, on the development of saline preference (salt appetite) in rats. Male Wistar rats were given a normal diet (1% NaCl) for 15 days and tested for salt appetite using a two-bottle choice test, one bottle containing water and the other 0.3 M saline. The animals were then divided into three groups (n = 11/group): one group received low NaCl, another received a Na(+)-deficient, normal-Cl-diet (low Na+), and a third received a Cl(-)-deficient, normal-Na+ diet (low Cl-). Salt appetite was again tested after 19 days on these diets. Both NaCl and Na+ depletion stimulated saline intake (P less than 0.01), whereas salt appetite did not change in the low-Cl- group. Water intake was not influenced by the regimens. In addition, no alterations were noted for weight, systolic blood pressure, plasma Na+ concentration, or blood pH. Dietary Cl-depletion, however, significantly reduced plasma Cl- concentration (P less than 0.05), and reduced plasma potassium in relation to rats depleted in Na+ (P less than 0.05). Plasma renin activity and urinary aldosterone were elevated in low-NaCl and Na(+)-depleted rats relative to the Cl(-)-depleted group (P less than 0.05). These results suggest that salt appetite is increased by dietary Na+ deficiency but not by Cl- deficiency. Salt appetite may be controlled by central or peripheral systems specifically sensitive to Na+ or by hormonal changes characteristic of Na+ depletion, such as the activation of renin and aldosterone observed in the low-NaCl and low-Na+ groups.

Aldosterone↗
PubMed1988

Relation of endogenous systemic and brain angiotensin II, arginine vasopressin and prolactin with the genesis of salt appetite in cattle.

Angiotensin II (AII), arginine vasopressin (AVP) and prolactin (PRL) were measured by radioimmunoassay in plasma and cerebrospinal fluid (CSF) in concurrent daily samples from conscious unrestrained steers. Packed cell volume, [Na+] and osmolality were also measured from these samples. Salt appetite was assessed during a 5-min daily session of operant conditioning. Food and water was always available. Unilateral parotid duct fistulation was effected under xylazine analgesia and halothane/O2 anaesthesia. To prevent a sodium deficit developing from loss of [Na+] in the extruded saliva, 0.3 M NaHCO3 was available ad libitum so that each animal could ingest sufficiently to balance the salivary loss. A week later epidural cannulae were implanted in the cisternae magna using the same anaesthesia. Three days afterwards when the saliva [Na] was 78 mmol/1, the 0.3-M NaHCO3 supplement was withdrawn for 7 days so that sodium deficiency developed to a degree which evoked salt appetite. When the NaHCO3 supplement was restored ad libitum, all aspects of [Na+] deficiency and salt appetite were completely ameliorated within 2-3 days. Packed cell volume increased and body weight decreased (p less than 0.05) during depletion, but rapidly returned to normal on day 2 of repletion. Both plasma and CSF osmolality were reduced during depletion as were plasma [Na+] (p less than 0.01) and CSF [Na+] (p less than 0.001). From a basal value of 64.7 +/- 9.35 fmol/ml on day 0, plasma AII increased to 229.2 +/- 46.65 fmol/ml (p less than 0.001) on day 3, prior to the onset of salt appetite on days 4-7. In marked contrast to plasma AII during sodium depletion, CSF AII was unchanged during salt appetite. There was no correlation between plasma and CSF AII during behavioural salt appetite.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed2005

Endocannabinoids and food intake: newborn suckling and appetite regulation in adulthood.

The appetite-stimulating effects of the cannabis plant (Cannabis sativa) have been known since ancient times, and appear to be effected through the incentive and rewarding properties of foods. Investigations into the biological basis of the multiple effects of cannabis have yielded important breakthroughs in recent years: the discovery of two cannabinoid receptors in brain and peripheral organ systems, and endogenous ligands (endocannabinoids) for these receptors. These advances have greatly increased our understanding of how appetite is regulated through these endocannabinoid receptor systems. The presence of endocannabinoids in the developing brain and in maternal milk have led to evidence for a critical role for CB1 receptors in oral motor control of suckling during neonatal development. The endocannabinoids appear to regulate energy balance and food intake at four functional levels within the brain and periphery: (i) limbic system (for hedonic evaluation of foods), (ii) hypothalamus and hindbrain (integrative functions), (iii) intestinal system, and (iv) adipose tissue. At each of these levels, the endocannabinoid system interacts with a number of better known molecules involved in appetite and weight regulation, including leptin, ghrelin, and the melanocortins. Therapeutically, appetite stimulation by cannabinoids has been studied for several decades, particularly in relation to cachexia and malnutrition associated with cancer, acquired immunodeficiency syndrome, or anorexia nervosa. The recent advances in cannabinoid pharmacology may lead to improved treatments for these conditions or, conversely, for combating excessive appetite and body weight, such as CB1 receptor antagonists as antiobesity medications. In conclusion, the exciting progress in the understanding of how the endocannabinoid CB receptor systems influence appetite and body weight is stimulating the development of therapeutic orexigenic and anorectic agents. Furthermore, the role of cannabinoid CB1 receptor activation for milk suckling in newborns may open new doors toward understanding nonorganic failure-to-thrive in infants, who display growth failure without known organic cause.

Adult↗
PubMed2006

Ghrelin has partial or no effect on appetite, growth hormone, prolactin, and cortisol release in patients with anorexia nervosa.

CONTEXT: Anorexia nervosa (AN) is an eating disorder characterized by self-induced starvation. Gastric hormone ghrelin, potent orexigen, and natural GH secretagogue are increased in AN. Although exogenous ghrelin stimulates appetite, GH, prolactin, and cortisol release in humans, its effects have not been studied, during infusions, in AN patients. OBJECTIVE: The objective of the study was to determine the effects of ghrelin on appetite, sleepiness, and neuroendocrine responses in AN patients. DESIGN: This was an acute interventional study. SETTING: The study was based at a hospital. Investigated SUBJECTS: Twenty-five young women, including nine patients diagnosed with AN with very low body weight, six AN patients who partially recovered their body weight but were still amenorrheic, and 10 constitutionally thin female subjects, without history of eating disorder, weight loss, with regular menstrual cycles, were included in the study. INTERVENTION: Each patient received 300-min iv infusion of ghrelin 5 pmol/kg.min and was asked to complete Visual Analog Scale questionnaires hourly. MAIN OUTCOME MEASURES: Visual Analog Scale scores for appetite and sleepiness, GH, prolactin, and cortisol responses were measured. RESULTS: At baseline, AN patients had significantly higher ghrelin, GH, and cortisol levels and significantly lower leptin than constitutionally thin subjects. GH responses to ghrelin infusion were blunted in patients with AN. Ghrelin administration did not significantly affect appetite but tended to increase sleepiness in AN patients. CONCLUSIONS: Ghrelin is unlikely to be effective as a single appetite stimulatory treatment for patients with AN. Our results suggest that AN patients are less sensitive to ghrelin in terms of GH response and appetite than healthy controls. Ghrelin effects on sleep need further studies.

Adult↗
PubMed1993

Circadian rhythms of appetite at different stages of a weight loss programme.

A group of 28 healthy obese people (16 women, 12 men) rated their appetite each whole hour of the day during nine separate days at three different stages of a dietary intervention study of 24 weeks. The first stage was an introduction period of eight weeks in which subjects were weight stable. The second stage was a weight reduction period of 13 weeks in which subjects lost about 0.85 kg/week of body weight. In the third stage of three weeks subjects were weight stable again. The slimming diet, which contained predominantly sweet items, had an energy content which was 1000 kcal (4.2 MJ) below the individually estimated daily energy expenditure. The results showed that appetite for a meal increased in the first week of the weight reduction period of 13 weeks but returned to the baseline level within 4-8 weeks. Appetite for something savoury remained elevated during the entire weight reduction period, and returned to the baseline level in the stabilization period. Appetite for something sweet did not change. The circadian rhythms of the different types of appetite remained unchanged at all stages during the diet intervention programme. Different types of appetite (e.g. sweet, savoury) had different patterns over the day.

Adult↗
PubMed1993

Salt appetite: its neuroendocrine basis.

Based on the early work of Richter (1936), showing that the adrenalectomized rat kept itself alive by drinking hypertonic NaCl solutions, Epstein and Stellar (1955) demonstrated that that salt appetite was innate, not dependent on learning. A series of later papers by Epstein and his students made clear that in addition to the adrenal steroid, aldosterone, salt appetite depended upon the action of angiotensin II in the brain. Blocking either hormone in the brain reduced depletion-induced salt appetite in half; blocking both eliminated it. Two salt depletions enhanced depletion-induced salt appetite by nearly a factor of two even when the rats never had a chance to drink salt in the first depletion. With multiple depletions, need-free salt intake also increased when the rats were sodium replete, producing an chronic, elevated salt appetite. Strikingly, female rats drink almost twice as much as males and become more enhanced by prior depletions. The neural circuitry involved in the synergy of angiotensin and aldosterone is becoming clearer with lesions of the amygdala that reduce aldosterone's effects and lesions of the anterior wall of the third ventricle that reduce angiotensin's effects. The significance of salt appetite in nature, in body fluid homeostasis, and as a model system of the brain mechanisms of ingestive behavior is discussed.

Animals↗
PubMed1987

Decrease of brain extracellular fluid [Na] and its interaction with other factors influencing sodium appetite in sheep.

It has been shown previously in sheep that physiological increase of cerebrospinal fluid (CSF) [Na] by infusion of 0.5 M NaCl artificial CSF causes a large reduction of sodium appetite of the sodium-deplete animal. Equivalent increase of CSF osmotic pressure caused by infusion 0.7 M mannitol artificial CSF which lowers CSF [Na] causes a doubling of sodium appetite. The results of the experiments here show that simple dilution of CSF [Na] with isotonic mannitol CSF, as distinct from use of hypertonic 0.7 M mannitol CSF, is an equally effective strong stimulus of sodium appetite. Lowering CSF [Na] concentration stimulates salt appetite in the severely sodium-deplete as well as in the mild to moderately sodium-deplete animal, and the effect of decrease of CSF [Na] on sodium appetite is sustained over 48 h. In addition, i.c.v. infusion of angiotensin II for the preceding 22 h at a rate which is an effective stimulus of both water and sodium solution intake in the sodium-replete animal, in fact, significantly decreased the sodium appetite stimulating effect of reduction of CSF [Na] in the Na-deplete animal.

Angiotensin II↗
PubMed2002

Co-occurrence of disturbed sleep and appetite loss differentiates between unipolar and bipolar depressive episodes.

The aim of this study was to examine whether the co-occurrence of disturbed sleep and appetite loss, two commonly encountered somatic symptoms of depression, can differentiate the clinical expression of depressive episodes between bipolar (BP) and unipolar patients (UP). Forty BP and 40 UP outpatients were interviewed through the Schedules for the Clinical Assessment in Neuropsychiatry (SCAN) and the presence of sleep disturbance and appetite loss during their most severe depressive episode was determined. Other variables studied were patients' gender and age, clinical characteristics related to the course of the disease (age at onset, duration of illness, and number and frequency of depressive and manic episodes), severity of the worst major depressive episode, and presence or absence of certain associated symptoms during that episode (loss of energy, low interest, feelings of guilt and/or self-reproach, impaired concentration, suicidal ideation, and agitation or retardation). Appetite loss was found to be more frequently present in UP (78%) than BP patients (55%, P<.05). No significant difference in the occurrence of sleep disturbance was found between the two groups. Among BP patients, appetite loss was present in 73% of those with sleep disturbance vs. 33% of those without (P<.02), while no such difference in co-occurrence of sleep disturbance and appetite loss was noticed among UP patients (74% vs. 85%, respectively, n.s.); this finding did not seem to be related to differences in severity of depression among UP and BP patients. Furthermore, those BP patients with co-occurrence of the two somatic symptoms complained also of loss of energy and low interest more often than those without (P<.01 and P<.05, respectively). No similar differences were observed among UP patients. The results of the present study suggest that the pathophysiological mechanisms underlying depressive episodes may differ between BP and UP affective disorder, and that those BP patients with simultaneous occurrence of sleep disturbance and appetite loss can be considered to belong to a particular nosologic subgroup with potential therapeutic and prognostic implications.

Adult↗
PubMed1992

Central oxytocin mediates inhibition of sodium appetite by naloxone in hypovolemic rats.

Pituitary oxytocin (OT) secretion is inversely related to saline consumption in several experimental models of sodium appetite in rats. Because systemic OT administration does not inhibit sodium appetite, release of OT as a neurotransmitter within the brain, coincident with its secretion from the pituitary, may be related to inhibition of sodium ingestion. The present studies evaluated this possibility by increasing brain OT concentrations both exogenously and endogenously in rats with hypovolemia produced by subcutaneous administration of polyethylene glycol (PEG) solution. Intracerebroventricular (i.c.v.) administration of OT completely abolished intake of 0.5 M NaCl in PEG-treated hypovolemic rats, but did not significantly affect PEG-stimulated water intakes. Endogenous OT secretion was stimulated by systemic treatment with naloxone, which has been shown to increase peripheral and central OT levels. In both one-bottle (0.5 M NaCl) and two-bottle (water and 0.5 M NaCl) drinking tests, intraperitoneal naloxone completely abolished sodium appetite in association with markedly increased pituitary secretion of OT. This inhibition of sodium appetite could be prevented by i.c.v. pretreatment with a specific OT-receptor antagonist, although the antagonist by itself did not affect PEG-stimulated sodium intake. These findings therefore support previous reports which have found that sodium appetite in rats is inhibited by treatments that elicit pituitary release of OT, and provide more direct evidence that brain OT is causally involved in the inhibition of sodium appetite stimulated by such treatments in rats.

Animals↗
PubMed1997

Neuroscience and appetitive behavior research: 25 years.

Neuroscience techniques have made major contributions to the understanding of appetitive behavior. Highlights in six areas are summarized to illustrate progress during the 25 years of the Columbia Appetitive Behavior Seminar: (1) discovery of angiotensin and aldosterone in the control of thirst and salt appetite; (2) electrophysiological decoding of chemoreceptive information in the brain; (3) a new foundation in the hypothalamus built on peptides, such as neuropeptide Y and galanin, interacting with monoamines and steroids in the control of appetite for macronutrients; (4) discovery of numerous peptides that mediate and integrate satiety, such as cholecystokinin, insulin, leptin and enterostatin, and other systems that suppress eating during illness; (5) better understanding of appetite suppressant drugs, and (6) exploration of a circuit that translates hypothalamic signals into behavioral action through connections to brainstem reflex arcs and forebrain instrumental response systems.

Appetite↗
PubMed2004

Investigation into the role of cephalic stimulation of acid secretion on gastric emptying and appetite following a soup meal using the gastric acid inhibitor omeprazole.

We previously showed that oral administration of a liquid soup preload was associated with a slower rate of gastric emptying and suppressed appetite more compared with intragastric administration of the same soup [Appetite 31(1998)377]. The present study was designed to investigate whether these results could be explained by the cephalic stimulation of acid secretion induced by oral administration. Eight healthy male subjects took part in a double-blind placebo controlled study comparing the effects of omeprazole and placebo on gastric emptying, appetite ratings and subsequent food intake following the ingestion of a liquid soup. Subjects were administered with a single oral dose of 80 mg omeprazole or placebo 3 h prior to ingesting the radiolabelled soup preload (400 kcal; 425 ml) over 15 min. Ratings of hunger, desire to eat and fullness were recorded over 135 min and gastric emptying was measured by scintigraphy. Food intake was evaluated from a test meal (yoghurt drink) given 120 min after the end of the soup ingestion. Analysis of data showed that there was no significant difference between omeprazole and placebo in gastric emptying, appetite or subsequent energy intake from the test meal. The results suggest that gastric acid secretion is not responsible for the differences in gastric emptying and appetite observed between intragastrically infused and orally administered soup preloads.

Administration, Oral↗
PubMed2002

Intake inhibition by NPY: role of appetitive ingestive behavior and aversion.

Intraventricular infusion of neuropeptide Y (NPY) decreases the amount female rats ingest during intraoral infusion (consummatory behavior) of a 1-M solution of sucrose at a rate of 0.5 ml/min and simultaneously increases the number of times the rats visit a bottle filled with sucrose (appetitive behavior). In this study, we investigated if the suppression of consummatory behavior was dependent upon the increase of appetitive behavior. The shift from consummatory to appetitive ingestive behavior was attenuated by adding 3-mM quinine HCl (QHCl) to the sucrose solution in the bottle. However, the intraoral intake of the sucrose solution was still decreased in NPY-treated rats. NPY did not modify taste reactivity as measured by aversive responses during continuous intraoral infusion of sucrose or ingestive and aversive responses to brief intraoral infusion of sucrose (0, 0.3 or 1 M) or QHCl (0, 0.3 or 3 mM). NPY stimulated visits to a bottle and intake from the bottle and inhibited sexual behavior in male rats but had no effect on the sexual behavior in the absence of a bottle. The visits and the intake were suppressed, but sexual behavior was not activated by adding QHCl (3 mM) to the solution in the bottle. Obstructing appetitive ingestive behavior, therefore, does not indiscriminately facilitate consummatory behavior. Male rats showed aversive or ingestive behavior and sexual behavior simultaneously during intraoral infusion of QHCl or condensed milk. It is suggested that NPY decreases intraoral intake and increases appetitive ingestive behavior via partially separable mechanisms that are independent of taste aversion.

Animals↗
PubMed2003

Short-term effects of sibutramine (Reductil) on appetite and eating behaviour and the long-term therapeutic outcome.

OBJECTIVE: To evaluate the short-term effects of sibutramine on appetite and eating behaviour and whether these effects are related to the long-term therapeutic outcome. STUDY DESIGN: Short-term: randomised, double-blind, placebo-controlled, within-subject design. Long-term: prospective open clinical trial. SUBJECTS: A total of 36 obese (nine men/27 women) with a body mass index of 39.3+/-4.3 (mean+/-s.d.) (range 30.2 - 45.2) kg/m(2) and age 44.4+/-12.1 y. PROCEDURE AND METHODS:: First phase-short-term effects: At baseline, the subjects were treated for 14 days with 15 mg sibutramine/placebo (period 1) followed by a 2 weeks single-blind placebo washout period, the subjects received the alternative therapy for another 14 days (period 2). At baseline, and at day 14 in each treatment period the subjects arrived fasting to the laboratory for a standardised breakfast and an ad libitum standardised lunch using the VIKTOR set-up (a universal eating monitor) to evaluate the microstructure of the eating behaviour (ie amount of food consumed and eating rate). Visual Analogue Scales were applied before and after the meals as well as every hour between the meals to monitor the appetite. During this first phase, subjects were encouraged to keep their habitual eating habits. Second phase-long-term effects: All subjects received 10 months open treatment with 15 mg sibutramine and dietary advice in monthly group sessions with a dietitian. On the last day of this treatment period, the subjects returned to repeat the measurements of appetite and eating behaviour using the same test procedure as during the first phase of the study. RESULTS: First phase: Sibutramine influenced appetite and eating behaviour that could be registered after only 14 days of treatment. The amount of food consumed at lunch on VIKTOR was reduced by 16% by sibutramine compared to placebo, 335+/-123 g vs 399+/-126 g (P<0.0001). Second phase: Responders and nonresponders were defined as those who ate less vs more food on VIKTOR when treated with sibutramine compared to the baseline food intake in the first phase of the study. The weight reduction was greater for responders 11.8+/-6.2 (mean+/-s.d.) kg compared to nonresponders 6.8+/-2.7 (mean+/-s.d.) kg (P<0.05). CONCLUSION: Short-term effects of sibutramine on appetite and eating behaviour were identified such as a reduction in food intake and in ratings of subjective motivation to eat. Short-term sibutramine effects on eating behaviour are to some extent related to the long-term therapeutic outcome in obese subjects.

Adult↗
PubMed1999

Mechanisms of uremic suppression of appetite.

Food intake is regulated by short-term satiety factors (gastric distension, amino acids, peptide hormones), as well as factors involved in long-term appetite regulation (leptin, insulin). Integration of the various signals takes place in the central nervous system (CNS). Appetite suppression in uremia is multifactorial and may include effects of uremia per se and of various comorbidity and psychosocial factors. Uremic anorexia is associated with elevated levels in plasma and CNS of short-term satiety factors (cholecystokinine, glucagon, serotonin, middle molecules) and factors that influence long-range regulation of appetite (leptin, insulin), but it is still unsettled to what extent these factors cause or contribute to appetite loss in uremic patients. Proinflammatory cytokines most probably also have a role in appetite suppression and malnutrition in patients with chronic renal failure.

Appetite↗
PubMed1995

Validity and epidemiology of reported poor appetite among Peruvian infants from a low-income, periurban community.

To assess the validity of maternal reports of poor infant appetite, these histories were compared with measured energy consumption on 1621 d of observation of 131 Peruvian infants in a low-income community. Mean (+/- SD) total energy intakes on days with reported anorexia were 338 +/- 88 kJ/kg body wt in infants 1-6 mo of age and 299 +/- 92 kJ/kg body wt in infants aged > 6 mo compared with 395 +/- 92 and 342 +/- 88 kJ/kg body wt in the respective age groups when appetites were reportedly normal (P < 0.001). Energy intake from non-breast-milk sources was more affected than energy from breast milk. The epidemiology of poor appetite was assessed in 153 infants who were monitored longitudinally during their first year of life. The prevalence of reported anorexia increased progressively from 22 to 317/1000 d of observation from < 1 to 11 mo of age. Infant age and the presence of fever, diarrhea, and respiratory illnesses were each associated negatively with the presence of reduced appetite. Poor appetite, rather than lack of food, may explain in part the low energy intakes by infants in this community.

Anorexia↗
PubMed1991

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.

Administration, Oral↗