Caregivers' Attention Toward, and Response to, Their Child's Interoceptive Hunger and Thirst Cues.

People can use their internal state to determine if they are hungry or thirsty. Although the meaning of some interoceptive cues may be innate (e.g., pain), it is possible that others-including those for hunger and thirst-are acquired. There has been little exploration of this idea in humans. Consequently, we conducted a survey among child caregivers to determine if the basic conditions necessary for interoceptive learning were present. Two-hundred and thirty-five caregivers of children aged 1-12 years were asked if they had recently noticed stomach rumbling, hunger-related irritability, and a dry mouth in their child. They were also asked how they would respond. The impact of several moderating variables, especially caregiver beliefs about the causes of hunger, fullness, and thirst, was also explored. Fifteen percent of caregivers had recently noticed stomach rumbling in their child, 28% hunger-related irritability, and 14% a dry mouth. Forty-four percent of caregivers had noticed at least one of these three cues. Noticing hunger cues was significantly moderated by caregiver beliefs about their cause, by child age, and in one case by temporal context (around vs. outside mealtimes). Key caregiver responses were providing the need (e.g., offer food) and/or asking the child if they had a need (e.g., hungry?). Each type of response could potentially support a different form of interoceptive learning. In conclusion, we suggest the necessary conditions for children to learn interoceptive hunger and thirst cues, are present in many caregiver-offspring dyads.

Safety and feasibility of early drinking water after general anesthesia recovery in patients undergoing daytime surgery.

BACKGROUND: Patients who are recovering from general anesthesia commonly exhibit symptoms such as dry lips, throat irritation, and thirst, prompting a desire to drink water in the post-anesthesia care unit (PACU). In this study, we aimed to evaluate the therapeutic effects and any potential complications of administering varying quantities of water to such patients. The primary objectives are to assess the safety and feasibility of early water intake after general anesthesia, specifically in the context of daytime surgery. METHODS: A total of 200 nongastrointestinal patients who underwent outpatient surgery were randomly assigned to four groups: Group A (drinking < 1 ml/kg), Group B (drinking 1-2 ml/kg), Group C (drinking > 2 ml/kg), and Group D (no water intake). We monitored changes in the assessment parameters before and after water consumption, as well as the incidence of post-drinking nausea and vomiting, and compared these outcomes among the four groups. RESULTS: Water intake led to a significant reduction in thirst, oropharyngeal discomfort, and pain scores and a notable increase in the gastric antrum motility index (MI), exhibiting statistical significance compared to the values before drinking (p < 0.05). Remarkably, higher water consumption correlated with enhanced gastrointestinal peristalsis. There was a significant difference in the antral MI among groups B, C, and A (p < 0.05). The occurrence of nausea and vomiting did not significantly differ among groups A, B, C, and D (p > 0.05). Early water consumption enhanced patient satisfaction with medical care, significantly varying from Group D (p < 0.05). CONCLUSION: Non-gastrointestinal surgical patients who passed pre-drinking water assessments post GA(general anesthesia)recovery could safely ingest moderate amounts of water in the PACU. Early water intake is both safe and feasible, effectively fostering swift postoperative recovery.

Reward value and internal state differentially drive impulsivity and motivation.

Goal-directed behavior is influenced by both reward value as well as internal state. A large body of research has focused on how reward value and internal drives such as hunger influence motivation in rodent models, however less work has focused on how these factors may differentially affect impulsivity. In these studies, we tested the effect of internal drive versus reward value on different facets of reward-related behavior including impulsive action, impulsive choice and, motivation. We varied reward value by changing the concentration of sucrose in the reward outcome, and varied internal drive by manipulating thirst through water restriction. Consistent with the literature we found that both internal state and reward value influenced motivation. However, we found that in high effort paradigms, only internal state influenced motivation with minimal effects of reward value. Interestingly, we found that internal state and reward value differentially influence different subtypes of impulsivity. Internal state, and to a lesser extent, reward value, influenced impulsive action as measured by premature responding. On the other hand, there were minimal effects of either reward value or homeostatic state on impulsive choice as measured by delay discounting. Overall, these studies begin to address how internal state and reward value differentially drive impulsive behavior. Understanding how these factors influence impulsivity is important for developing behavioral interventions and treatment targets for patients with dysregulated motivated or impulsive behavior.

An integrative sensor of body states: how the mushroom body modulates behavior depending on physiological context.

The brain constantly compares past and present experiences to predict the future, thereby enabling instantaneous and future behavioral adjustments. Integration of external information with the animal's current internal needs and behavioral state represents a key challenge of the nervous system. Recent advancements in dissecting the function of the Drosophila mushroom body (MB) at the single-cell level have uncovered its three-layered logic and parallel systems conveying positive and negative values during associative learning. This review explores a lesser-known role of the MB in detecting and integrating body states such as hunger, thirst, and sleep, ultimately modulating motivation and sensory-driven decisions based on the physiological state of the fly. State-dependent signals predominantly affect the activity of modulatory MB input neurons (dopaminergic, serotoninergic, and octopaminergic), but also induce plastic changes directly at the level of the MB intrinsic and output neurons. Thus, the MB emerges as a tightly regulated relay station in the insect brain, orchestrating neuroadaptations due to current internal and behavioral states leading to short- but also long-lasting changes in behavior. While these adaptations are crucial to ensure fitness and survival, recent findings also underscore how circuit motifs in the MB may reflect fundamental design principles that contribute to maladaptive behaviors such as addiction or depression-like symptoms.

Fluid transitions.

Water is critical for survival and thirst is a powerful way of ensuring that fluid levels remain in balance. Overconsumption, however, can have deleterious effects, therefore optimization requires a need to balance the drive for water with the satiation of that water drive. This review will highlight our current understanding of how thirst is both generated and quenched, with particular focus on the roles of angiotensin II, glucagon like-peptide 1, and estradiol in turning on and off the thirst drive. Our understanding of the roles these bioregulators play has benefited from modern behavioral analyses, which have improved the time resolution of intake measures, allowing for attention to the details of the patterns within a bout of intake. This has led to behavioral interpretation in ways that are helpful in understanding the many controls of water intake and has expanded our understanding beyond the dichotomy that something which increases water intake is simply a "stimulator" while something that decreases water intake is simply a "satiety" factor. Synthesizing the available information, we describe a framework in which thirst is driven directly by perturbations in fluid intake and indirectly modified by several bioregulators. This allows us to better highlight areas that are in need of additional attention to form a more comprehensive understanding of how the system transitions between states of thirst and satiety.

The relationship between fatigue, pruritus, and thirst distress with quality of life among patients receiving hemodialysis: a mediator model to test concept of treatment adherence.

Hemodialysis is a conservative treatment for end-stage renal disease. It has various complications which negatively affect quality of life (QOL). This study aimed to examine the relationship between fatigue, pruritus, and thirst distress (TD) with QOL of patients receiving hemodialysis, while also considering the mediating role of treatment adherence (TA). This cross-sectional study was carried out in 2023 on 411 patients receiving hemodialysis. Participants were consecutively recruited from several dialysis centers in Iran. Data were collected using a demographic information form, the Fatigue Assessment Scale, the Thirst Distress Scale, the Pruritus Severity Scale, the 12-Item Short Form Health Survey, and the modified version of the Greek Simplified Medication Adherence Questionnaire for Hemodialysis Patients. Covariance-based structural equation modeling was used for data analysis. The structural model and hypothesis testing results showed that all hypotheses were supported in this study. QOL had a significant inverse association with fatigue, pruritus, and TD and a significant positive association with TA. TA partially mediated the association of QOL with fatigue, pruritus, and TD, denoting that it helped counteract the negative association of these complications on QOL. This model explained 68.5% of the total variance of QOL. Fatigue, pruritus, and TD have a negative association with QOL among patients receiving hemodialysis, while TA reduces these negative associations. Therefore, TA is greatly important to manage the associations of these complications and improve patient outcomes. Healthcare providers need to assign high priority to TA improvement among these patients to reduce their fatigue, pruritus, and TD and improve their QOL. Further studies are necessary to determine the most effective strategies for improving TA and reducing the burden of complications in this patient population.

Acute hypernatremia increases functional connectivity of NaCl sensing regions in the human brain: An fMRI pilot study.

Rodent studies demonstrated specialized sodium chloride (NaCl) sensing neurons in the circumventricular organs, which mediate changes in sympathetic nerve activity, arginine vasopressin, thirst, and blood pressure. However, the neural pathways involved in NaCl sensing in the human brain are incompletely understood. The purpose of this pilot study was to determine if acute hypernatremia alters the functional connectivity of NaCl-sensing regions of the brain in healthy young adults. Resting-state fMRI scans were acquired in 13 participants at baseline and during a 30 min hypertonic saline infusion (HSI). We used a seed-based approach to analyze the data, focusing on the subfornical organ (SFO) and the organum vasculosum of the lamina terminalis (OVLT) as regions of interest (ROIs). Blood chemistry and perceived thirst were assessed pre- and post-infusion. As expected, serum sodium increased from pre- to post-infusion in the HSI group. The primary finding of this pilot study was that the functional connectivity between the SFO and a cluster within the OVLT increased from baseline to the late-phase of the HSI. Bidirectional connectivity changes were found with cortical regions, with some regions showing increased connectivity with sodium-sensing regions while others showed decreased connectivity. Furthermore, the functional connectivity between the SFO and the posterior cingulate cortex (a control ROI) did not change from baseline to the late-phase of the HSI. This finding indicates a distinct response within the NaCl sensing network in the human brain specifically related to acute hypernatremia that will need to be replicated in large-scale studies.

Non-pharmacological interventions to reduce thirst in patients with heart failure or hemodialysis: A systematic review and meta-analysis.

BACKGROUND: Thirst is a frequent and burdening symptom in many patients, especially in patients with chronic heart failure (CHF) and/or receiving hemodialysis (HD). As drug therapies are not feasible, non-pharmacological strategies are needed to reduce thirst and thirst-related burden. OBJECTIVES: To identify non-pharmacological interventions aiming to reduce thirst in patients with CHF and/ or HD, to describe intervention components, and to evaluate the effectiveness of these interventions. METHODS: In February 2024, we completed a systematic search in MEDLINE via PubMed, Livivo, CINAHL, Cochrane Library and Web of Science. Two reviewers independently screened titles, abstracts, and full texts, performed critical appraisal and data extraction. We checked risk of bias with the checklists of the Joanna Briggs Institute and the Cochrane Risk of Bias tool and calculated meta-analyses for sufficiently homogeneous studies using fixed-effects models. RESULTS: We included 15 intervention studies applying non-pharmacological interventions including chewing gum (n = 8), low-sodium diet (n = 2), acupressure (n = 1), frozen strawberries (n = 1), fluid timetables (n = 1), ice cubes and mouthwash (n = 1), and a psychological intervention (n = 1). Sample sizes varied between 11 and 88 participants. Eleven intervention studies showed a reduction of thirst as intervention effect. Meta-analyses for chewing gum showed no significant effect on thirst using a visual analogue scale (IV: -2,32 [-10.37,5.73]; p = 0.57) or the dialysis thirst inventory (IV: -0.26 [- 1.83, 1.30]; p = 0.74). Quality of studies was moderate to low. CONCLUSION: Results indicate that various non-pharmacological interventions could be helpful to reduce thirst in patients with CHF or HD, but important uncertainty remains.

Brain sodium sensing for regulation of thirst, salt appetite, and blood pressure.

The brain possesses intricate mechanisms for monitoring sodium (Na) levels in body fluids. During prolonged dehydration, the brain detects variations in body fluids and produces sensations of thirst and aversions to salty tastes. At the core of these processes Nax , the brain's Na sensor, exists. Specialized neural nuclei, namely the subfornical organ (SFO) and organum vasculosum of the lamina terminalis (OVLT), which lack the blood-brain barrier, play pivotal roles. Within the glia enveloping the neurons in these regions, Nax collaborates with Na+ /K+ -ATPase and glycolytic enzymes to drive glycolysis in response to elevated Na levels. Lactate released from these glia cells activates nearby inhibitory neurons. The SFO hosts distinct types of angiotensin II-sensitive neurons encoding thirst and salt appetite, respectively. During dehydration, Nax -activated inhibitory neurons suppress salt-appetite neuron's activity, whereas salt deficiency reduces thirst neuron's activity through cholecystokinin. Prolonged dehydration increases the Na sensitivity of Nax via increased endothelin expression in the SFO. So far, patients with essential hypernatremia have been reported to lose thirst and antidiuretic hormone release due to Nax -targeting autoantibodies. Inflammation in the SFO underlies the symptoms. Furthermore, Nax activation in the OVLT, driven by Na retention, stimulates the sympathetic nervous system via acid-sensing ion channels, contributing to a blood pressure elevation.

Human hunger as a memory process.

Hunger refers to (1) the meaning of certain bodily sensations; (2) a mental state of anticipation that food will be good to eat; and (3) an organizing principal, which prioritizes feeding. Definitions (1) and (2) are the focus here, as (3) can be considered their consequent. Definition (1) has been linked to energy-depletion models of hunger, but these are no longer thought viable. Definition (2) has been linked to learning and memory (L&M) models of hunger, but these apply just to palatable foods. Nonetheless, L&M probably forms the basis for hunger generally, as damage to declarative memory can eradicate the experience of hunger. Currently, there is no general L&M model of hunger, little understanding of how physiology intersects with a L&M approach, and no understanding of how Definitions (1) and (2) are related. We present a new L&M model of human hunger. People learn associations between internal (e.g., tummy rumbles) and external cues (e.g., brand names) and food. These associations can be to specific foods (episodic memories) or food-related categories (semantic memories). When a cue is encountered, it may lead to food-related memory retrieval. If retrieval occurs, the memory's affective content allows one to know if food will be good to eat now-hunger-a cognitive operation learned in childhood. These memory processes are acutely inhibited during satiety, and chronically by multiple biological parameters, allowing physiology to modulate hunger. Implications are considered for the process of making hunger judgments, thirst, the cephalic phase response, and motivational and lay theories of hunger. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Two parabrachial Cck neurons involved in the feedback control of thirst or salt appetite.

Thirst and salt appetite are temporarily suppressed after water and salt ingestion, respectively, before absorption; however, the underlying neural mechanisms remain unclear. The parabrachial nucleus (PBN) is the relay center of ingestion signals from the digestive organs. We herein identify two distinct neuronal populations expressing cholecystokinin (Cck) mRNA in the lateral PBN that are activated in response to water and salt intake, respectively. The two Cck neurons in the dorsal-lateral compartment of the PBN project to the median preoptic nucleus and ventral part of the bed nucleus of the stria terminalis, respectively. The optogenetic stimulation of respective Cck neurons suppresses thirst or salt appetite under water- or salt-depleted conditions. The combination of optogenetics and in vivo Ca2+ imaging during ingestion reveals that both Cck neurons control GABAergic neurons in their target nuclei. These findings provide the feedback mechanisms for the suppression of thirst and salt appetite after ingestion.

Neural landscape diffusion resolves conflicts between needs across time.

Animals perform flexible goal-directed behaviours to satisfy their basic physiological needs1-12. However, little is known about how unitary behaviours are chosen under conflicting needs. Here we reveal principles by which the brain resolves such conflicts between needs across time. We developed an experimental paradigm in which a hungry and thirsty mouse is given free choices between equidistant food and water. We found that mice collect need-appropriate rewards by structuring their choices into persistent bouts with stochastic transitions. High-density electrophysiological recordings during this behaviour revealed distributed single neuron and neuronal population correlates of a persistent internal goal state guiding future choices of the mouse. We captured these phenomena with a mathematical model describing a global need state that noisily diffuses across a shifting energy landscape. Model simulations successfully predicted behavioural and neural data, including population neural dynamics before choice transitions and in response to optogenetic thirst stimulation. These results provide a general framework for resolving conflicts between needs across time, rooted in the emergent properties of need-dependent state persistence and noise-driven shifts between behavioural goals.

Dopaminergic error signals retune to social feedback during courtship.

Hunger, thirst, loneliness and ambition determine the reward value of food, water, social interaction and performance outcome1. Dopamine neurons respond to rewards meeting these diverse needs2-8, but it remains unclear how behaviour and dopamine signals change as priorities change with new opportunities in the environment. One possibility is that dopamine signals for distinct drives are routed to distinct dopamine pathways9,10. Another possibility is that dopamine signals in a given pathway are dynamically tuned to rewards set by the current priority. Here we used electrophysiology and fibre photometry to test how dopamine signals associated with quenching thirst, singing a good song and courting a mate change as male zebra finches (Taeniopygia guttata) were provided with opportunities to retrieve water, evaluate song performance or court a female. When alone, water reward signals were observed in two mesostriatal pathways but singing-related performance error signals were routed to Area X, a striatal nucleus specialized for singing. When courting a female, water seeking was reduced and dopamine responses to both water and song performance outcomes diminished. Instead, dopamine signals in Area X were driven by female calls timed with the courtship song. Thus the dopamine system handled coexisting drives by routing vocal performance and social feedback signals to a striatal area for communication and by flexibly re-tuning to rewards set by the prioritized drive.

Sodium appetite and thirst do not require angiotensinogen production in astrocytes or hepatocytes.

In addition to its renal and cardiovascular functions, angiotensin signalling is thought to be responsible for the increases in salt and water intake caused by hypovolaemia. However, it remains unclear whether these behaviours require angiotensin production in the brain or liver. Here, we use in situ hybridization to identify tissue-specific expression of the genes required for producing angiotensin peptides, and then use conditional genetic deletion of the angiotensinogen gene (Agt) to test whether production in the brain or liver is necessary for sodium appetite and thirst. In the mouse brain, we identified expression of Agt (the precursor for all angiotensin peptides) in a large subset of astrocytes. We also identified Ren1 and Ace (encoding enzymes required to produce angiotensin II) expression in the choroid plexus, and Ren1 expression in neurons within the nucleus ambiguus compact formation. In the liver, we confirmed that Agt is widely expressed in hepatocytes. We next tested whether thirst and sodium appetite require angiotensinogen production in astrocytes or hepatocytes. Despite virtually eliminating expression in the brain, deleting astrocytic Agt did not reduce thirst or sodium appetite. Despite markedly reducing angiotensinogen in the blood, eliminating Agt from hepatocytes did not reduce thirst or sodium appetite, and in fact, these mice consumed the largest amounts of salt and water after sodium deprivation. Deleting Agt from both astrocytes and hepatocytes also did not prevent thirst or sodium appetite. Our findings suggest that angiotensin signalling is not required for sodium appetite or thirst and highlight the need to identify alternative signalling mechanisms. KEY POINTS: Angiotensin signalling is thought to be responsible for the increased thirst and sodium appetite caused by hypovolaemia, producing elevated water and sodium intake. Specific cells in separate brain regions express the three genes needed to produce angiotensin peptides, but brain-specific deletion of the angiotensinogen gene (Agt), which encodes the lone precursor for all angiotensin peptides, did not reduce thirst or sodium appetite. Double-deletion of Agt from brain and liver also did not reduce thirst or sodium appetite. Liver-specific deletion of Agt reduced circulating angiotensinogen levels without reducing thirst or sodium appetite. Instead, these angiotensin-deficient mice exhibited an enhanced sodium appetite. Because the physiological mechanisms controlling thirst and sodium appetite continued functioning without angiotensin production in the brain and liver, understanding these mechanisms requires a renewed search for the hypovolaemic signals necessary for activating each behaviour.

La sed ¿un mecanismo suficiente para lograr euhidratación?: una revisión narrativa / Is thirst sufficient as a mechanism for achieving euhydration? a narrative review

Capitán, C. y Aragón, L.F. (2023). La sed ¿un mecanismo suficiente para lograr euhidratación?: una revisión narrativa. PENSAR EN MOVIMIENTO: Revista de Ciencias del Ejercicio y la Salud, 21(1), 1-16. El papel de la percepción de sed para mantener el balance hídrico ha sido ampliamente estudiado, tanto durante el ejercicio como después de este. Sin embargo, la forma de evaluarla y la eficacia de los instrumentos existentes son aún áreas que necesitan más investigación. El objetivo de esta revisión fue integrar, de forma general, la información disponible en la literatura sobre el funcionamiento del mecanismo de la sed como respuesta a la deshidratación durante y después del ejercicio. Se explican los mecanismos fisiológicos y las respuestas de estos durante y posterior al ejercicio; además, se describen los instrumentos disponibles en la literatura científica, sus debilidades y fortalezas, y se plantea una serie de preguntas que aún no tienen respuesta en el área. En esta revisión se presenta el aspecto teórico de los mecanismos de la sed, además, se discuten los estudios científicos que respaldan o refutan el comportamiento de estos mecanismos en el ejercicio. Finalmente, se hace un resumen de las principales conclusiones extraídas de la literatura científica sobre la sed como un mecanismo suficiente para prevenir la deshidratación tanto durante como después del ejercicio.

Capitán, C. y Aragón, L.F. (2023). Is thirst sufficient as a mechanism for achieving euhydration? a narrative review. PENSAR EN MOVIMIENTO: Revista de Ciencias del Ejercicio y la Salud, 21(1), 1-16. The role of thirst perception for keeping hydric balance, both during and after exercise, has been extensively studied. However, the way to assess it and the effectiveness of the existing instruments are areas that still require further research. The objective of this review is to integrate, in a general way, the information available in the literature on the functioning of the thirst mechanism as a response to dehydration during and after exercise. The physiological mechanisms and their responses during and after exercise are explained. In addition, a description of the instruments available in scientific literature is included, together with their weaknesses and strengths, and a series of as yet unanswered questions in this area are raised. This review presents the theoretical aspect of thirst mechanisms, and discusses the scientific studies that support or refute the behavior of these mechanisms in exercise. Finally, a summary is made of the major conclusions drawn from the scientific literature on thirst as a sufficient mechanism to prevent dehydration both during and after exercise.

Capitán, C. y Aragón, L.F. (2023). A sede é um mecanismo suficiente para alcançar a hidratação? uma revisão narrativa. PENSAR EN MOVIMIENTO: Revista de Ciencias del Ejercicio y la Salud, 21(1), 1-16. O papel da percepção da sede na manutenção do equilíbrio hídrico tem sido amplamente estudado, tanto durante quanto após o exercício. Entretanto, como avaliá-la e a eficácia dos instrumentos existentes ainda são áreas que necessitam de mais pesquisas. Esta revisão visou integrar, de forma geral, as informações disponíveis na literatura sobre o funcionamento do mecanismo da sede em resposta à desidratação durante e após o exercício. Ele explica os mecanismos fisiológicos e suas respostas durante e após o exercício, descreve os instrumentos disponíveis na literatura científica, seus pontos fracos e fortes, e levanta uma série de questões que permanecem sem resposta no campo. Esta revisão apresenta o aspecto teórico dos mecanismos da sede e discute os estudos científicos que respaldam ou refutam o comportamento desses mecanismos no exercício. Finalmente, é feito um resumo das principais conclusões extraídas da literatura científica sobre a sede como mecanismo suficiente para prevenir a desidratação tanto durante quanto após o exercício.

WNK1 promotes water homeostasis by acting as a central osmolality sensor for arginine vasopressin release.

Maintaining internal osmolality constancy is essential for life. Release of arginine vasopressin (AVP) in response to hyperosmolality is critical. Current hypotheses for osmolality sensors in circumventricular organs (CVOs) of the brain focus on mechanosensitive membrane proteins. The present study demonstrated that intracellular protein kinase WNK1 was involved. Focusing on vascular-organ-of-lamina-terminalis (OVLT) nuclei, we showed that WNK1 kinase was activated by water restriction. Neuron-specific conditional KO (cKO) of Wnk1 caused polyuria with decreased urine osmolality that persisted in water restriction and blunted water restriction-induced AVP release. Wnk1 cKO also blunted mannitol-induced AVP release but had no effect on osmotic thirst response. The role of WNK1 in the osmosensory neurons in CVOs was supported by neuronal pathway tracing. Hyperosmolality-induced increases in action potential firing in OVLT neurons was blunted by Wnk1 deletion or pharmacological WNK inhibitors. Knockdown of Kv3.1 channel in OVLT by shRNA reproduced the phenotypes. Thus, WNK1 in osmosensory neurons in CVOs detects extracellular hypertonicity and mediates the increase in AVP release by activating Kv3.1 and increasing action potential firing from osmosensory neurons.

Thirst: neuroendocrine regulation in mammals.

Animals can sense their changing internal needs and then generate specific physiological and behavioural responses in order to restore homeostasis. Water-saline homeostasis derives from balances of water and sodium intake and output (drinking and diuresis, salt appetite and natriuresis), maintaining an appropriate composition and volume of extracellular fluid. Thirst is the sensation which drives to seek and consume water, regulated in the central nervous system by both neural and chemical signals. Water and electrolyte homeostasis depends on finely tuned physiological mechanisms, mainly susceptible to plasma Na+ concentration and osmotic pressure, but also to blood volume and arterial pressure. Increases of osmotic pressure as slight as 1-2% are enough to induce thirst ("homeostatic" or cellular), by activation of specialized osmoreceptors in the circumventricular organs, outside the blood-brain barrier. Presystemic anticipatory signals (by oropharyngeal or gastrointestinal receptors) inhibit thirst when fluids are ingested, or stimulate thirst associated with food intake. Hypovolemia, arterial hypotension, Angiotensin II stimulate thirst ("hypovolemic thirst", "extracellular dehydration"). Hypervolemia, hypertension, Atrial Natriuretic Peptide inhibit thirst. Circadian rhythms of thirst are also detectable, driven by suprachiasmatic nucleus in the hypothalamus. Such homeostasis and other fundamental physiological functions (cardiocircolatory, thermoregulation, food intake) are highly interdependent.

Age-Associated Abnormalities of Water Homeostasis.

Deficits in renal function, thirst, and responses to osmotic and volume stimulation have been repeatedly demonstrated in older populations. The lessons learned over the past six decades serve to emphasize the fragile nature of water balance characteristic of aging. Older individuals are at increased risk for disturbances of water homeostasis due to both intrinsic disease and iatrogenic causes. These disturbances have real-life clinical implications in terms of neurocognitive effects, falls, hospital readmission and need for long-term care, incidence of bone fracture, osteoporosis, and mortality.