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At least 73 records · Page 4Linked to original sources
PubMed1985

The effect of captopril on sodium appetite in adrenalectomized and deoxycorticosterone-treated rats.

Captopril caused a renin-dependent increase in water intake in rats with bilateral ureteric ligation. But despite the fluid retention and fall in osmolality caused by the increased water intake, rats with ureteric ligation did not drink the 2.7% NaCl also offered to them. In rats with a pre-existing increase in sodium appetite caused by adrenalectomy, low dosage of captopril augmented intake of both water and 2.7% NaCl whereas high dosage inhibited intake of both fluids after an initial increase in water intake. In contrast, rats with a pre-existing increase in sodium appetite caused by daily injections of deoxycorticosterone showed no changes in intake of water or 2.7% NaCl after either low or high dosage of captopril, though they drank both fluids after intracranial injection of angiotensin II. Increases in water and 2.7% NaCl intake caused by low dosage of captopril in adrenalectomized rats were not secondary to increased urinary fluid and electrolyte losses. Decreases in intake after high dosage were not explained by the rats being too weak to drink. Low and high dosage of captopril caused increases in plasma renin concentration in adrenalectomized rats, but in contrast renin remained undetectable in the plasma of deoxycorticosterone-treated rats after the highest dosage of captopril. Whether or not captopril affected a pre-existing sodium appetite depended on whether or not it increased plasma renin. Since it affected the pre-existing sodium appetite and plasma renin in the adrenalectomized rat but neither of these in the deoxycorticosterone-treated rat, it is likely that the appetite was renin-dependent in the former but not in the latter. Because captopril only affected thirst in the rat with ligated ureters whereas it affected both sodium appetite and thirst in the adrenalectomized rat, increases in renal renin secretion alone may not be enough to stimulate sodium appetite. The additional stimulus provided by adrenalectomy, or the absence of some inhibitory factor that may be present after ureteric ligation, is also needed.

Adrenalectomy↗
PubMed1998

Effect of glucose supplementation on appetite and the pyloric motor response to intraduodenal glucose and lipid.

The effects of different macronutrients on appetite and pyloric motility and the impact of short-term dietary glucose supplementation on these responses were evaluated. Ten males (aged 19-38 yr) received isocaloric (2.9 kcal/min) intraduodenal infusions of glucose and lipid while antropyloroduodenal motility and appetite were assessed by manometry and visual analog scales, respectively. Effects of each intraduodenal nutrient on appetite and motility were evaluated before and after 7 days of dietary supplementation with glucose (400 g daily). Initially, both nutrients caused a similar rise in pyloric tone, but intraduodenal lipid was a more potent stimulus of phasic pyloric motility (P = 0.05) and suppressed appetite more (P = 0.013) than intraduodenal glucose. After dietary glucose supplementation, the increase in pyloric tone during intraduodenal glucose was attenuated. Although intraduodenal lipid remained a more potent stimulant of phasic pyloric motility (P = 0.016), it no longer decreased appetite. We conclude that in healthy young males 1) intraduodenal infusion of lipid is a more potent stimulus of phasic pyloric motility and suppresses appetite more than intraduodenal glucose and 2) dietary glucose supplementation alters both the appetite suppressant effect of intraduodenal lipid and the pyloric motor response to intraduodenal glucose infusion.

Adult↗
PubMed1985

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.

Adrenalectomy↗
PubMed2000

Circumventricular organs and ANG II-induced salt appetite: blood pressure and connectivity.

A lesion of the subfornical organ (SFO) may reduce sodium depletion-induced salt appetite, which is largely dependent on ANG II, and yet ANG II infusions directly into SFO do not provoke salt appetite. Two experiments were designed to address this apparent contradiction. In experiment 1 sustained infusions of ANG II into SFO did not produce a sustained elevation of blood pressure, and neither a reduction of blood pressure alone with minoxidil and captopril nor a reduction of both blood pressure and volume with furosemide and captopril enhanced salt appetite. Infusions of ANG II in the organum vasculosum laminae terminalis (OVLT) did evoke salt appetite without raising blood pressure. In experiment 2 knife cuts of the afferent and efferent fibers of the rostroventral pole of the SFO abolished water intake during an infusion of ANG II into the femoral vein but failed to reduce salt appetite during an infusion of ANG II into the OVLT. We conclude that 1) hypertension does not account for the failure of infusions of ANG II in the SFO to generate salt appetite and 2) the OVLT does not depend on its connectivity with the SFO to generate salt appetite during ANG II infusions.

Angiotensin II↗
PubMed1998

Angiotensin, thirst, and sodium appetite.

Angiotensin (ANG) II is a powerful and phylogenetically widespread stimulus to thirst and sodium appetite. When it is injected directly into sensitive areas of the brain, it causes an immediate increase in water intake followed by a slower increase in NaCl intake. Drinking is vigorous, highly motivated, and rapidly completed. The amounts of water taken within 15 min or so of injection can exceed what the animal would spontaneously drink in the course of its normal activities over 24 h. The increase in NaCl intake is slower in onset, more persistent, and affected by experience. Increases in circulating ANG II have similar effects on drinking, although these may be partly obscured by accompanying rises in blood pressure. The circumventricular organs, median preoptic nucleus, and tissue surrounding the anteroventral third ventricle in the lamina terminalis (AV3V region) provide the neuroanatomic focus for thirst, sodium appetite, and cardiovascular control, making extensive connections with the hypothalamus, limbic system, and brain stem. The AV3V region is well provided with angiotensinergic nerve endings and angiotensin AT1 receptors, the receptor type responsible for acute responses to ANG II, and it responds vigorously to the dipsogenic action of ANG II. The nucleus tractus solitarius and other structures in the brain stem form part of a negative-feedback system for blood volume control, responding to baroreceptor and volume receptor information from the circulation and sending ascending noradrenergic and other projections to the AV3V region. The subfornical organ, organum vasculosum of the lamina terminalis and area postrema contain ANG II-sensitive receptors that allow circulating ANG II to interact with central nervous structures involved in hypovolemic thirst and sodium appetite and blood pressure control. Angiotensin peptides generated inside the blood-brain barrier may act as conventional neurotransmitters or, in view of the many instances of anatomic separation between sites of production and receptors, they may act as paracrine agents at a distance from their point of release. An attractive speculation is that some are responsible for long-term changes in neuronal organization, especially of sodium appetite. Anatomic mismatches between sites of production and receptors are less evident in limbic and brain stem structures responsible for body fluid homeostasis and blood pressure control. Limbic structures are rich in other neuroactive peptides, some of which have powerful effects on drinking, and they and many of the classical nonpeptide neurotransmitters may interact with ANG II to augment or inhibit drinking behavior. Because ANG II immunoreactivity and binding are so widely distributed in the central nervous system, brain ANG II is unlikely to have a role as circumscribed as that of circulating ANG II. Angiotensin peptides generated from brain precursors may also be involved in functions that have little immediate effect on body fluid homeostasis and blood pressure control, such as cell differentiation, regeneration and remodeling, or learning and memory. Analysis of the mechanisms of increased drinking caused by drugs and experimental procedures that activate the renal renin-angiotensin system, and clinical conditions in which renal renin secretion is increased, have provided evidence that endogenously released renal renin can generate enough circulating ANG II to stimulate drinking. But it is also certain that other mechanisms of thirst and sodium appetite still operate when the effects of circulating ANG II are blocked or absent, although it is not known whether this is also true for angiotensin peptides formed in the brain. Whether ANG II should be regarded primarily as a hormone released in hypovolemia helping to defend the blood volume, a neurotransmitter or paracrine agent with a privileged role in the neural pathways for thirst and sodium appetite of all kinds, a neural organizer especially in sodium appetit

Angiotensin II↗
PubMed2006

Appearance-specific satiety increases appetite and quality of life in patients with metastatic liver tumor: a case report.

Loss of appetite is frequently seen and is a main factor affecting quality of life (QOL) in patients with advanced cancer. The etiology for loss of appetite in patients with cancer is multifactorial. The sensory properties of food are factors regulating appetite. Changes in taste, smell and texture of foods influence food intake. The appearance of the food is also a notable factor in sensory-specific satiety. We described a 46-year-old Japanese woman with multiple metastatic liver tumors. Although there was no obvious factor for loss of appetite, she suffered from a loss of appetite and subsequent malnutrition. In order to improve the appearance of food, we reduced the diet to 1,000 kcal/day from 1,500 kcal/day. On the new diet, the patient's appetite significantly increased and patient's nutritional status was improved. Eating whole diet was an important achievement and increased in mental aspects of QOL. Arrangement for the appearance of food may be a simple and nontoxic therapeutic strategy for patients with cancer suffering a loss of appetite.

Appetite↗
PubMed2000

Quality of life and stimulation of weight gain after treatment with megestrol acetate: correlation between cytokine levels and nutritional status, appetite in geriatric patients with wasting syndrome.

BACKGROUND: The geriatric wasting syndrome (GWS) has been associated with proinflammatory cytokines, depression and progressive decline in quality of life (QOL). The objective of this study was to evaluate the correlation between the changes in cytokine levels and appetite, nutritional markers, and QOL in geriatric patients with GWS following a randomized clinical trial of megestrol acetate (MA) versus placebo. METHODS: This was a prospective, double-blind, placebo-controlled trial. We evaluated 69 predominantly male (3 females) nursing home residents with weight loss of > or =5% of their usual body weight over the past three months or body weight 20% below their ideal body weight. Patients were randomly assigned to receive either placebo or megestrol acetate (MA) oral suspension (O.S.) 800 mg/day for 12 weeks and were then followed for 13 weeks off treatment. Data on appetite, weight, nutritional status, QOL and cytokine levels were collected at baseline and week 12. The correlation between appetite, weight, nutritional status, sense of well being and cytokine level changes in response to MA treatment was examined at week 12. RESULTS: Appetite, sense of well being, and QOL assessed by an "enjoyment list" significantly improved in the MA arm. Rising prealbumin showed a negative correlation with decreasing IL-6 (r = -0.51), TNFR-p 55 (r = -0.49) and sIL-2R (r = -0.38). There was also an improvement in prealbumin and a decrease in IL-6 and TNFR-p55 in the MA-arm (p < 0.01). A correlation between a decrease in the IL-6 levels and improvement in depression (r = 0.50) was seen in the MA arm as well. Improvement in appetite positively correlated with increased enjoyment of life (r = -0.41), less depression (r = -0.34), improved sense of well being (r = 0.36), prealbumin gain (r = 0.30), and weight gain (r = 0.38) by 12 weeks. Also, improvement in appetite positively correlated with improvement in nutritional parameters such as prealbumin, albumin, fat free mass and weight in the MA arm. CONCLUSIONS: In a geriatric nursing home population with weight loss, reduction in cytokine levels after MA treatment correlates with improvement in appetite, prealbumin, albumin, and improvement in quality of life.

Aged↗
PubMedDate not supplied

The Functional Assessment of Anorexia/Cachexia Therapy (FAACT) Appetite Scale in veteran cancer patients.

Anorexia and appetite assessment is an important priority in supportive oncology. A series of 156 veterans participating in a hematology oncology service completed the Functional Assessment of Anorexia/Cachexia Therapy (FAACT), the Functional Assessment of Cancer Therapy-General scale, the Memorial Symptom Assessment Scale Short Form (MSAS-SF), and the Zung Self-Rating Depression Scale and were followed for survival. The FAACT score correlated well with Karnofsky performance status, quality of life, and symptom distress subscales. A single appetite distress item from the MSAS-SF correlated well with these measures. Both appetite measures correlated with the presence of other symptoms and with concurrently measured hemoglobin, serum sodium, albumin, and cholesterol levels. These self-reported appetite measures were univariate predictors of survival and contributed additional prognostic information to data related to weight-loss distress. In a smaller study, the FAACT score correlated with a visual analogue measure of appetite and with the North Center Cancer Treatment Group appetite instrument. These data support use of these tools for the evaluation of appetite concerns among patients with advanced cancer.

Adult↗
PubMed1982

Appetite for vitamin C: its relationship to cellular energy potential.

Appetite for vitamin C varies between individuals who consume it for control of inflammatory respiratory, and central nervous symptoms, all of which may have an allergic etiology. The mechanisms affecting appetite for vitamin C are discussed. Ascorbic acid is involved in the appreciation of taste which is diminished in allergic disease, as is appetite in scorbutic conditions. The actions of some appetite-depressant drugs such as fenfluramine, are reduced by administration of vitamin C. It appears that appetite diminished when brain ascorbic levels are reduced below a critical level. When tissue ascorbic acid concentrations are reduced, cellular electric potential is diminished. Cellular electric potential is diminished in allergic disease concurrently with development of symptoms. It is suggested that patho-physiological changes in the nervous system may occur in consequence of increased utilisation of ascorbic acid resulting from allergic and iatrogenic challenge. Appetite for vitamin C would be then be affected on an idiosyncratic basis. It is possible that this appetite is controlled by a neurological feed-back mechanism, activation of which is determined by reduction in cellular electric potential of tissues depleted by ascorbic acid.

Absorption↗
PubMed1999

Performance of appetitive or consummatory components of male sexual behavior is mediated by different brain areas: a 2-deoxyglucose autoradiographic study.

The in vivo autoradiographic deoxyglucose method was used to identify the functional brain circuits that are involved in the performance of appetitive and consummatory components of male sexual behavior in Japanese quail (Coturnix japonica). Two groups of castrated, testosterone-treated male quail were trained during 12 sessions to associate the view of a female behind a window with the opportunity to interact freely and to copulate with her. They developed, as a consequence, a social proximity response (staying close and looking through the window providing a view of the female) that has been used in previous experiments to measure appetitive sexual behavior. A third control group (also castrated and treated with testosterone) was allowed to view the female but not to copulate with her and therefore did not develop this proximity response. 2-14C-deoxyglucose was then injected i.p. to these birds and they were allowed to either copulate freely with a female (consummatory sexual behavior group) or express the social proximity response (appetitive sexual behavior group). The control group was provided a view of the female but these birds, although they were exposed to the same stimuli as birds in the appetitive group, did not express the social proximity response because they had never learned the association with the opportunity to copulate. Birds were killed 45 min after the deoxyglucose injection and their brains were processed for autoradiography. Densitometric analyses of the autoradiograms revealed that the expression of appetitive or consummatory aspects of male sexual behavior was associated with significant increases by comparison with the control group in the deoxyglucose incorporation in the nucleus mesencephalicus lateralis, pars dorsalis and in the nucleus leminsci lateralis. In addition, an increase in the deoxyglucose incorporation was specifically observed in the paleostriatum primitivum, rostral preoptic area, nucleus intercollicularis, nucleus interpeduncularis and third nerve but a decrease was observed in the dorsomedial part of the hippocampus and in the nucleus nervi oculomotori in birds of the consummatory sexual behavior group by comparison with controls. By contrast, in the appetitive sexual behavior group, significant increases in deoxyglucose incorporation were observed in two telencephalic areas, the intermediate hyperstriatum ventrale and neostriatum caudolaterale by comparison with the controls, but decreases were detected in the stratum griseum et fibrosum superficiale of optic tectum by comparison with the consummatory behavior group. These studies demonstrate that the performance of appetitive or consummatory components of male sexual behavior affects in a specific manner the deoxyglucose uptake and accumulation in specific regions of the quail brain. Changes in metabolic activity were observed in steroid-sensitive areas, in auditory, visual and vocal brain regions, and in brain nuclei related to motor behavior but also in association telencephalic and limbic structures. These changes in oxidative metabolism overlap to some extent with metabolic changes as revealed by immunocytochemistry for the immediate early gene products Fos and Zenk, but many specific reactions are also detected indicating that these techniques are not necessarily redundant and, together, they can provide a more complete picture of the brain circuits that are implicated in the control and performance of complex behaviors.

Animals↗
PubMed1990

Appetite disturbance and the problems of overweight.

During the past 50 years, obesity has increasingly become a problem in Western societies. If low energy output by these individuals (i.e. lack of exercise) cannot be held totally accountable for this problem, then their energy input (i.e. appetite) must play a significant role. There are many elements that give rise to appetite disturbances and their effects on weight gain, weight loss or its maintenance. Previously, it was thought that emotional disturbances led to overeating and overweight; a theory that was supplanted later by the theory that physiological rather than psychological causes were to blame. Today, it is generally believed that appetite is controlled by the interaction of internal (genetic, physiological and chemical) and external (environmental and psychosocial) processes. The role of nutritional and dietary factors in controlling the expression of appetite are particularly important. Thus, appetite (hyperphagia or increased hunger) can be induced by changes in brain neurotransmitters and neuromodulators, altered liver metabolism, adjustments of the nutrient/sensory components of the diet, environmentally applied stressors, the mental and behavioural imposition of dieting and the administration of various psychotropic medications. This review focuses on the role of each of these mechanisms plays in the genesis and maintenance of appetite disturbances; the conclusion of each of these contributions is the same--control of appetite must be achieved in order to treat obesity, and to do this, control must be exerted via regulation of the food supply, cognitive methods, environmental adjustment or by pharmacological tools.

Feeding and Eating Disorders↗
PubMed2003

Maternal smoking during pregnancy and appetite control in offspring.

AIMS: Intrauterine exposure to tobacco smoke products has been associated with long-term neurobehavioral effects. Modified appetite control might explain the recently observed association between maternal smoking during pregnancy and obesity in offspring. METHODS: Some 10,557 British adults aged 42 years born between 3-9 March 1958 were followed up in a birth cohort study (NCDS). The main outcome measure was self-reported poor appetite at age 42 years and main exposure was maternal smoking during pregnancy. RESULTS: The proportion of offspring with poor appetite increased with maternal smoking during pregnancy: non-smoking 4.5%; (4.0%-5.0%), medium smoking 5.6%; (4.5%-6.8%), variable smoking 6.8%; (4.9%-9.1%) and heavy smoking 7.7%; (6.3%-9.4%). The unadjusted odds ratios for maternal smoking during pregnancy (ever/never) and poor appetite is 1.49 (1.25-1.77) and after adjustment for BMI at 42 years and other potential confounding factors it is 1.22 (1.01-1.48). CONCLUSIONS: Offspring of mothers who smoked during pregnancy were more likely to report a poor appetite independent of a number of potential confounding factors. Although not in the expected direction, the results suggest maternal smoking during pregnancy may influence appetite perception through a developmental influence or through confounding by social factors.

Adult↗
PubMed2004

The pharmacology of human appetite expression.

The discovery of the adiposity signal leptin a decade ago revolutionised our understanding of the hypothalamic mechanisms underpinning the central control of ingestive behaviour. Subsequently, the structure and function of various hypothalamic peptide systems (Neuropeptide Y (NPY), Orexins, Melanocortins, Cocaine and Amphetamine Regulating Transcript (CART), Galanin/Galanin Like Peptides (GALP) and endocannabinoids) have been characterised in detail in rodent models. The therapeutic benefit of targeting these systems remains to be discovered. More is becoming known about the pharmacological potential of peripheral, meal-induced, episodic endogenous peptides. Hormones such as Cholecystokinin (CCK), Gastrin Releasing Peptides (GRP), Glucagon-Like Peptide I (GLP-1) Enterostatin, Amylin, Peptide YY (PYY) and Ghrelin are released prior to, during and/or after a meal, controlling intake and subjective feelings of appetite (hunger and satiety). In addition, there is an expanding body of literature detailing the effects of a wide variety of drugs on human appetite and food intake. Some of these drugs act upon CNS monoamine systems such as Serotonin (5-HT). Dopamine (DA) and Noradrenaline (NA), have long been implicated in appetite regulation. Detailed examination of both the effect of agonising endogenous gut peptide systems and the effect of various monoaminergic drugs on the expression of human appetite can provide a greater understanding of mechanisms underpinning normal appetite regulation. However, such an understanding must be based on knowledge of the effect of the treatment on meal size, eating rate, meal pattern, food choice and the subjective experience of appetite flux (hunger and satiety), and notjust food intake.

Appetite↗
PubMed1990

Analysis of associative learning in the terrestrial mollusc Limax maximus. II. Appetitive learning.

The odor and taste processing systems of the terrestrial mollusc Limax maximus have been shown capable of a number of complex computations. Most of the complex higher-order features of Limax learning have been demonstrated using differential aversive conditioning. The present experiments probe the appetitive learning ability of Limax. In the first experiment a differential appetitive classical conditioning procedure was used. An aversive CS+ odor was paired with an attractive taste while a CS- odor was explicitly unpaired with the attractive taste. This appetitive conditioning procedure dramatically increased the preference for the CS+ odor. Further experiments determined the time course of acquisition, the effect of an extinction procedure and long-term retention of the appetitive conditioning. Now that Limax has been shown capable of appetitive conditioning, the neural network simulation of Limax learning, called LIMAX, can be examined for its ability to display appetitive conditioning.

Animals↗
PubMedDate not supplied

Lesions of the rat nucleus basalis magnocellularis disrupt appetitive-to-aversive transfer learning.

Rats with selective lesions of the nucleus basalis magnocellularis (NBM) and sham-lesion control animals were tested in an operant appetitive-to-aversive transfer task. We hypothesized that NBM lesions would not affect performance in the appetitive phase, but that performance would be impaired during subsequent transfer to the aversive phase of the task. Additional groups of NBM lesion and control rats were tested in the avoidance condition only, where we hypothesized that NBM lesions would not disrupt performance. These hypotheses were based on the argument that the NBM is not necessary for simple association learning that does not tax attention. Both the appetitive phase of the transfer task and the avoidance only task depend only on simple associative learning and are argued not to tax attention. Consequently, performance in these tasks was predicted to be spared following NBM lesions. Complex, attention-demanding associative learning, however, is argued to depend on the NBM. Performance in the aversive phase of the transfer task is both attentionally demanding and associatively more complex than in either the appetitive or aversive tasks alone; thus, avoidance performance in the NBM lesion group was predicted to be impaired following transfer from prior appetitive conditioning. Results supported our hypotheses, with the NBM lesion group acquiring the appetitive response normally, but showing impaired performance following transfer to the aversive conditioning phase of the transfer task. Impairments were not attributable to disrupted avoidance learning per se, as avoidance behavior was normal in the NBM lesion group tested in the avoidance condition only.

Analysis of Variance↗
PubMed1991

Effect of the 5-HT2 antagonist ketanserin on salt appetite in the rat.

The 5-HT2 antagonist ketanserin inhibited salt appetite induced by subchronic deoxycorticosterone acetate (DOCA) treatment, as well as salt appetite induced by sodium depletion (which is governed by the synergy of aldosterone and angiotensin in the brain). The effect of ketanserin was more evident following intraperitoneal than intracerebroventricular injection. On the other hand, ketanserin did not inhibit either salt intake induced by intracranial renin injection, or the need-free salt intake of the multidepleted female rat, which is not dependent on the renin-angiotensin-aldosterone system. These findings suggest that the antinatriorexic action of ketanserin is selective for the mineralcorticoid mechanisms controlling salt appetite. Ritanserin, too, a potent 5-HT2 antagonist showing a different receptor selectivity profile from that of ketanserin, suppressed DOCA-induced salt appetite, thus supporting the involvement of 5-HT receptors in the antinatriorexic action. DOCA treatment alters serotonin metabolism in the central nervous system and it has been proposed that changes in 5-HT metabolism may be important in the genesis of DOCA-induced hypertension. The present results indicate that ketanserin inhibits DOCA-induced salt appetite and suggest that serotoninergic mechanisms might be involved in the elicitation of mineralocorticoid-induced salt appetite.

Animals↗
PubMedDate not supplied

Cortisol measures in primary major depressive disorder with hypersomnia or appetite increase.

Morning plasma cortisol response to the 1 mg dexamethasone suppression test along with cortisol levels in blood, cerebrospinal fluid (CSF), and urine were measured in hospitalized male and female patients with primary major depressive disorder who reported hypersomnia (n = 23), or increase in appetite (n = 22). Comparisons were drawn to cortisol levels in patients with primary major depressive disorder who did not report hypersomnia or appetite increase (n = 23) and to normal controls (n = 23), all age- and sex-matched. Depressives with hypersomnia or increased appetite showed higher than normal 24-h urinary free cortisol concentrations. Depressed patients without hypersomnia or appetite increase had in addition to elevated free urinary cortisol concentrations higher than normal morning plasma cortisol levels before and after dexamethasone administration and a higher incidence of cortisol non-suppression after dexamethasone compared to normal subjects. The findings provide preliminary evidence that HPA activation in depression is diminished in the presence of hypersomnia and/or an increased appetite. Studies of the hypothalamic-pituitary-adrenal axis may be useful for differentiating subtypes of depression characterized by hypersomnia or enhanced appetite.

Adult↗
PubMed1996

Angiotensin II receptor subtype antagonists can both stimulate and inhibit salt appetite in rats.

In urethane-anaesthetised male Wistar rats iontophoretic application of the angiotensin II (Ang II) type 1 (AT-1) receptor specific nonpeptide antagonist losartan in the septo-preoptic continuum can produce neuronal excitation of short- and long-term duration which has been interpreted as removal of tonic Ang II-induced inhibition. Mineralocorticoid pretreatment, which increases neuronal sensitivity to Ang II to enhance salt appetite, also removes this losartan-induced long-term excitation. These results suggested steroid modulation of the AT-1 receptor and a complex involvement of Ang II in salt appetite. To investigate the role of the inhibitory action of central Ang II on salt appetite, we gave intracerebroventicular injections of a single, low dose (10 ng) of losartan in normal euhydrated rats and this produced, paradoxically, a progressive increase in salt intake (1.6 +/- 0.3 ml/day to 3.5 +/- 0.9 ml/day, n = 15, P < 0.05). Treatment of these salt enhanced rats with DOCA (0.5 mg/day, s.c., for 3 days) further increased the salt appetite, but then a second i.c.v. injection of the same dose of losartan significantly inhibited the enhanced salt appetite (4.7 +/- 0.7 to 1.3 +/- 0.4, n = 9, P < 0.05). These results provide evidence for a complex action of Ang II on the At-1 receptor mediating the generation of salt appetite that appears to involve either at least two functional subtypes of this AT-1 receptor, as already suggested by previous electrophysiological experiments, or one AT-1 receptor with several activation states.

Angiotensin II↗