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.

Comparison of dipsogenic responses of adult rat offspring as a function of different perinatal programming models.

The perinatal environment interacts with the genotype of the developing organism resulting in a unique phenotype through a developmental or perinatal programming phenomenon. However, it remains unclear how this phenomenon differentially affects particular targets expressing specific drinking responses depending on the perinatal conditions. The main goal of the present study was to compare the dipsogenic responses induced by different thirst models as a function of two perinatal manipulation models, defined by the maternal free access to hypertonic sodium solution and a partial aortic ligation (PAL-W/Na) or a sham-ligation (Sham-W/Na). The programmed adult offspring of both perinatal manipulated models responded similarly when was challenged by overnight water dehydration or after a sodium depletion showing a reduced water intake in comparison to the non-programmed animals. However, when animals were evaluated after a body sodium overload, only adult Sham-W/Na offspring showed drinking differences compared to PAL and control offspring. By analyzing the central neurobiological substrates involved, a significant increase in the number of Fos + cells was found after sodium depletion in the subfornical organ of both programmed groups and an increase in the number of Fos + cells in the dorsal raphe nucleus was only observed in adult depleted PAL-W/Na. Our results suggest that perinatal programming is a phenomenon that differentially affects particular targets which induce specific dipsogenic responses depending on matching between perinatal programming conditions and the osmotic challenge in the latter environment. Probably, each programmed-drinking phenotype has a particular set point to elicit specific repertoires of mechanisms to reestablish fluid balance.

The gut-brain axis and sodium appetite: Can inflammation-related signaling influence the control of sodium intake?

Sodium is the main cation present in the extracellular fluid. Sodium and water content in the body are responsible for volume and osmotic homeostasis through mechanisms involving sodium and water excretion and intake. When body sodium content decreases below the homeostatic threshold, a condition termed sodium deficiency, highly motivated sodium seeking, and intake occurs. This is termed sodium appetite. Classically, sodium and water intakes are controlled by a number of neuroendocrine mechanisms that include signaling molecules from the renin-angiotensin-aldosterone system acting in the central nervous system (CNS). However, recent findings have shown that sodium and water intakes can also be influenced by inflammatory agents and mediators acting in the CNS. For instance, central infusion of IL-1ß or TNF-α can directly affect sodium and water consumption in animal models. Some dietary conditions, such as high salt intake, have been shown to change the intestinal microbiome composition, stimulating the immune branch of the gut-brain axis through the production of inflammatory cytokines, such as IL-17, which can stimulate the brain immune system. In this review, we address the latest findings supporting the hypothesis that immune signaling in the brain could produce a reduction in thirst and sodium appetite and, therefore, contribute to sodium intake control.

Awareness of Fluid Losses Does Not Impact Thirst during Exercise in the Heat: A Double-Blind, Cross-Over Study.

BACKGROUND: Thirst has been used as an indicator of dehydration; however, as a perception, we hypothesized that it could be affected by received information related to fluid losses. The purpose of this study was to identify whether awareness of water loss can impact thirst perception during exercise in the heat. METHODS: Eleven males participated in two sessions in random order, receiving true or false information about their fluid losses every 30 min. Thirst perception (TP), actual dehydration, stomach fullness, and heat perception were measured every 30 min during intermittent exercise until dehydrated by ~4% body mass (BM). Post exercise, they ingested water ad libitum for 30 min. RESULTS: Pre-exercise BM, TP, and hydration status were not different between sessions (p > 0.05). As dehydration progressed during exercise, TP increased significantly (p = 0.001), but it was the same for both sessions (p = 0.447). Post-exercise water ingestion was almost identical (p = 0.949) in the two sessions. CONCLUSION: In this study, thirst was a good indicator of fluid needs during exercise in the heat when no fluid was ingested, regardless of receiving true or false water loss information.

Transcultural adaptation of the Thirst Distress Scale (TDS) into Brazilian Portuguese and an analysis of the psychometric properties of the scale for patients on hemodialysis / Adaptação transcultural do instrumento Thirst Distress Scale (TDS) para o português brasileiro e propriedades psicométricas em pacientes em hemodiálise

Abstract Objective: To produce a transcultural adaptation of the Thirst Distress Scale (TDS) into Brazilian Portuguese and analyze the scale's psychometric properties for patients on hemodialysis (HD). Methods: The original scale was translated, back translated, and discussed with psychometric assessment experts. The final version was tested with 126 patients on HD and retested with 70 individuals from the original patient population. Cronbach's alpha was used to measure the scale's internal consistency. Reliability of thirst intensity evaluated via the visual analogue scale (VAS) was tested with Kappa statistic and the Bland-Altman plot. Reproducibility was assessed based on the intraclass correlation coefficient (ICC). Results: The wording of three items and the verb tenses of six had to be adjusted in the final version of the Brazilian Portuguese TDS. Comprehension of the scale by patients on HD was good, the scale's internal consistency was satisfactory (0.84; p<0.001), agreement with a visual analogue scale (VAS) was moderate (kappa=0.44; p<0.001), and reproducibility neared perfection (ICC=0.87; p<0.001). Conclusion: Our results showed that the Brazilian Portuguese version of the scale might be used reliably. The Brazilian Portuguese version of the TDS is a practical, affordable, accessible and well-accepted tool that has a lot to offer for the management of patients with HD.

Resumo Objetivo: Realizar a adaptação transcultural da escala Thirst Distress Scale (TDS) para o português brasileiro e estudar suas propriedades psicométricas em pacientes em hemodiálise (HD). Métodos: Foram realizadas traduções, retrotraduções, discussão com especialistas e avaliação psicométrica, com aplicação da versão final em 126 pacientes em HD e reteste em 70 pacientes da amostra inicial. A consistência interna do instrumento foi obtida pelo alfa de Cronbach. Para analisar a concordância com a intensidade de sede, avaliada pela Escala Visual Analógica (EVA), foi utilizado o teste Kappa e a estratégia gráfica de Bland-Altman. Para avaliar a reprodutibilidade, foi realizado teste de correlação intraclasse (CCI). Resultados: Para obtenção da versão final da escala TDS em português brasileiro, intitulada TDS-BR, foi necessária adaptação de vocabulário em três itens e mudança de tempo verbal em seis itens. Houve boa compreensão da escala pelos pacientes em HD, consistência interna satisfatória (0,84, p<0,001), concordância moderada com a Escala Visual Analógica (EVA) (kappa=0,44; p<0,001) e reprodutibilidade quase perfeita (CCI=0,87; p<0,001). Conclusão: Os resultados obtidos indicam a aplicabilidade e confiabilidade do instrumento na língua portuguesa (Brasil). A ferramenta, por ser de fácil compreensão e baixo custo, além de ter boa aceitação, pode ser um instrumento relevante no manejo da sede de pacientes em HD.

Transcultural adaptation of the Thirst Distress Scale (TDS) into Brazilian Portuguese and an analysis of the psychometric properties of the scale for patients on hemodialysis.

OBJECTIVE: To produce a transcultural adaptation of the Thirst Distress Scale (TDS) into Brazilian Portuguese and analyze the scale's psychometric properties for patients on hemodialysis (HD). METHODS: The original scale was translated, back translated, and discussed with psychometric assessment experts. The final version was tested with 126 patients on HD and retested with 70 individuals from the original patient population. Cronbach's alpha was used to measure the scale's internal consistency. Reliability of thirst intensity evaluated via the visual analogue scale (VAS) was tested with Kappa statistic and the Bland-Altman plot. Reproducibility was assessed based on the intraclass correlation coefficient (ICC). RESULTS: The wording of three items and the verb tenses of six had to be adjusted in the final version of the Brazilian Portuguese TDS. Comprehension of the scale by patients on HD was good, the scale's internal consistency was satisfactory (0.84; p<0.001), agreement with a visual analogue scale (VAS) was moderate (kappa=0.44; p<0.001), and reproducibility neared perfection (ICC=0.87; p<0.001). CONCLUSION: Our results showed that the Brazilian Portuguese version of the scale might be used reliably. The Brazilian Portuguese version of the TDS is a practical, affordable, accessible and well-accepted tool that has a lot to offer for the management of patients with HD.

Brain osmo-sodium sensitive channels and the onset of sodium appetite.

The aim of the present study was to determine whether the TRPV1 channel is involved in the onset of sodium appetite. For this purpose, we used TRPV1-knockout mice to investigate sodium depletion-induced drinking at different times (2/24 h) after furosemide administration combined with a low sodium diet (FURO-LSD). In sodium depleted wild type and TRPV1 KO (SD-WT/SD-TPRV1-KO) mice, we also evaluated the participation of other sodium sensors, such as TPRV4, NaX and angiotensin AT1-receptors (by RT-PCR), as well as investigating the pattern of neural activation shown by Fos immunoreactivity, in different nuclei involved in hydromineral regulation. TPRV1 SD-KO mice revealed an increased sodium preference, ingesting a higher hypertonic cocktail in comparison with SD-WT mice. Our results also showed in SD-WT animals that SFO-Trpv4 expression increased 2 h after FURO-LSD, compared to other groups, thus supporting a role of SFO-Trpv4 channels during the hyponatremic state. However, the SD-TPRV1-KO animals did not show this early increase, and maybe as a consequence drank more hypertonic cocktail. Regarding the SFO-NaX channel expression, in both genotypes our findings revealed a reduction 24 h after FURO-LSD. In addition, there was an increase in the OVLT-NaX expression of SD-WT 24 h after FURO-LSD, suggesting the participation of OVLT-NaX channels in the appearance of sodium appetite, possibly as an anticipatory response in order to limit sodium intake and to induce thirst. Our work demonstrates changes in the expression of different osmo­sodium-sensitive channels at specific nuclei, related to the body sodium status in order to stimulate an adequate drinking.

Thirst Is Associated with Suppression of Habenula Output and Active Stress Coping: Is there a Role for a Non-canonical Vasopressin-Glutamate Pathway?

Water-homeostasis is a fundamental physiological process for terrestrial life. In vertebrates, thirst drives water intake, but the neuronal circuits that connect the physiology of water regulation with emotional context are poorly understood. Vasopressin (VP) is a prominent messenger in this circuit, as well as L-glutamate. We have investigated the role of a VP circuit and interaction between thirst and motivational behaviors evoked by life-threatening stimuli in rats. We demonstrate a direct pathway from hypothalamic paraventricular VP-expressing, glutamatergic magnocellular neurons to the medial division of lateral habenula (LHbM), a region containing GABAergic neurons. In vivo recording and juxtacellular labeling revealed that GABAergic neurons in the LHbM had locally branching axons, and received VP-positive axon terminal contacts on their dendrites. Water deprivation significantly reduced freezing and immobility behaviors evoked by innate fear and behavioral despair, respectively, accompanied by decreased Fos expression in the lateral habenula. Our results reveal a novel VP-expressing hypothalamus to the LHbM circuit that is likely to evoke GABA-mediated inhibition in the LHbM, which promotes escape behavior during stress coping.

Mapping brain Fos immunoreactivity in response to water deprivation and partial rehydration: Influence of sodium intake.

Water deprivation (WD) followed by water intake to satiety, produces satiation of thirst and partial rehydration (PR). Thus, WD-PR is a natural method to differentiate thirst from sodium appetite. WD-PR also produces Fos immunoreactivity (Fos-ir) in interconnected areas of a brain circuit postulated to subserve sodium appetite. In the present work, we evaluated the effect of sodium intake on Fos-ir produced by WD-PR in brain areas operationally defined according to the literature as either facilitatory or inhibitory to sodium intake. Isotonic NaCl was available for ingestion in a sodium appetite test performed immediately after a single episode of WD-PR. Sodium intake decreased Fos-ir in facilitatory areas such as the lamina terminalis (particularly subfornical organ and median preoptic nucleus), central amygdala and hypothalamic parvocellular paraventricular nucleus in the forebrain. Sodium intake also decreased Fos-ir in inhibitory areas such as the area postrema, lateral parabrachial nucleus and nucleus of the solitary tract in the hindbrain. In contrast, sodium intake further increased Fos-ir that was activated by water deprivation in the dorsal raphe nucleus, another inhibitory area localized in the hindbrain. WD-PR increased Fos-ir in the core and shell of the nucleus accumbens. Sodium intake reduced Fos-ir in both parts of the accumbens. In summary, sodium intake following WD-PR reduced Fos-ir in most facilitatory and inhibitory areas, but increased Fos-ir in another inhibitory area. It also reduced Fos-ir in a reward area (accumbens). The results suggest a functional link between sodium intake and the activity of the hindbrain-forebrain circuitry subserving reward and sodium appetite in response to water deprivation.

Hydrogen peroxide attenuates the dipsogenic, renal and pressor responses induced by cholinergic activation of the medial septal area.

Cholinergic activation of the medial septal area (MSA) with carbachol produces thirst, natriuresis, antidiuresis and pressor response. In the brain, hydrogen peroxide (H2O2) modulates autonomic and behavioral responses. In the present study, we investigated the effects of the combination of carbachol and H2O2 injected into the MSA on water intake, renal excretion, cardiovascular responses and the activity of vasopressinergic and oxytocinergic neurons in the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei. Furthermore, the possible modulation of carbachol responses by H2O2 acting through K+ATP channels was also investigated. Male Holtzman rats (280-320 g) with stainless steel cannulas implanted in the MSA were used. The pre-treatment with H2O2 in the MSA reduced carbachol-induced thirst (7.9±1.0, vs. carbachol: 13.2±2.0 ml/60 min), antidiuresis (9.6±0.5, vs. carbachol: 7.0±0.8 ml/120 min,), natriuresis (385±36, vs. carbachol: 528±46 µEq/120 min) and pressor response (33±5, vs. carbachol: 47±3 mmHg). Combining H2O2 and carbachol into the MSA also reduced the number of vasopressinergic neurons expressing c-Fos in the PVN (46.4±11.2, vs. carbachol: 98.5±5.9 c-Fos/AVP cells) and oxytocinergic neurons expressing c-Fos in the PVN (38.5±16.1, vs. carbachol: 75.1±8.5 c-Fos/OT cells) and in the SON (57.8±10.2, vs. carbachol: 102.7±7.4 c-Fos/OT cells). Glibenclamide (K+ATP channel blocker) into the MSA partially reversed H2O2 inhibitory responses. These results suggest that H2O2 acting through K+ATP channels in the MSA attenuates responses induced by cholinergic activation in the same area.

Role of thirst and visual barriers in the differential behavior displayed by streptozotocin-treated rats in the elevated plus-maze and the open field test.

Conflicting results have been obtained by several groups when studying the effects of streptozotocin (STZ)-treated rats in the elevated plus-maze (EPM). Since thirst is a prominent feature in STZ-induced diabetic-like condition, we studied whether the walls of the closed arms of the EPM, by limiting the search for water in the environment, may contribute to the observed differential behavioral outcomes. The aim of this study was to ascertain whether visual barriers within the EPM have an influence on the behavior of STZ-treated rats in this test of anxiety. A striking similarity between STZ-treated (50 mg/kg, i.p., in two consecutive days) and water deprived rats (72 h) was found in exploratory behavior in the EPM, showing an anxiolytic-like profile. However the anxiolytic response of STZ-treated rats exposed to the EPM shifts into an anxiogenic profile when they are subsequently tested in the open-field test, which unlike the EPM is devoid of visual barriers. Likewise, water deprived rats (72 h) also showed an anxiogenic profile when they were exposed to the open-field test. Our results indicate that experimental outcomes based on EPM observations can be misleading when studying physiological or pathological conditions, e.g. diabetes, in which thirst may increase exploratory behavior.

Ontogenetic role of angiontensin-converting enzyme in rats: thirst and sodium appetite evaluation.

We investigated the influence of captopril (an angiotensin converting enzyme inhibitor) treatment during pregnancy and lactation period on hydromineral balance of the male adult offspring, particularly, concerning thirst and sodium appetite. We did not observe significant alterations in basal hydromineral (water intake, 0.3M NaCl intake, volume and sodium urinary concentration) or cardiovascular parameters in adult male rats perinatally treated with captopril compared to controls. However, male offspring rats that perinatally exposed to captopril showed a significant attenuation in water intake induced by osmotic stimulation, extracellular dehydration and beta-adrenergic stimulation. Moreover, captopril treatment during perinatal period decreased the salt appetite induced by sodium depletion. This treatment also attenuated thirst and sodium appetite aroused during inhibition of peripheral angiotensin II generation raised by low concentration of captopril in the adult offspring. Interestingly, perinatal exposure to captopril did not alter water or salt intake induced by i.c.v. administration of angiotensin I or angiotensin II. These results showed that chronic inhibition of angiotensin converting enzyme during pregnancy and lactation modifies the regulation of induced thirst and sodium appetite in adulthood.

Drinking policies and exercise-associated hyponatraemia: is anyone still promoting overdrinking?

OBJECTIVES: The purpose of this review is to describe the evolution of hydration research and advice on drinking during exercise from published scientific papers, books and non-scientific material (advertisements and magazine contents) and detail how erroneous advice is likely propagated throughout the global sports medicine community. DESIGN: Hydration advice from sports-linked entities, the scientific community, exercise physiology textbooks and non-scientific sources was analysed historically and compared with the most recent scientific evidence. CONCLUSIONS: Drinking policies during exercise have changed substantially throughout history. Since the mid-1990s, however, there has been an increase in the promotion of overdrinking by athletes. While the scientific community is slowly moving away from "blanket" hydration advice in which one form of advice fits all and towards more modest, individualised, hydration guidelines in which thirst is recognised as the best physiological indicator of each subject's fluid needs during exercise, marketing departments of the global sports drink industry continue to promote overdrinking.

Oestrogenic influence on brain AT1 receptor signalling on the thirst and sodium appetite in osmotically stimulated and sodium-depleted female rats.

The present work was carried out to investigate the role of angiotensin II type 1 (AT(1)) receptors in nocturnal thirst and sodium appetite induced by classical models of osmotic and sodium depletion challenges in ovariectomized rats chronically treated with oil or oestradiol benzoate (EB, 20 microg per animal, s.c. daily). In both conditions, the animals were given saline or losartan (108 nmol per animal, i.c.v.), a selective AT(1) receptor blocker. Oestrogen therapy significantly reduced the water intake induced by water deprivation, sodium depletion produced by frusemide injected 24 h before, and s.c. acute frusemide plus captopril injection (FUROCAP protocol), with no alteration following s.c. hypertonic saline injection. In contrast, EB therapy decreased the salt intake induced by sodium depletion and FUROCAP protocols, with no alteration following water deprivation and s.c. hypertonic saline injection. Central AT(1) blockade inhibited the dipsogenic response induced by water deprivation, osmotic stimulation, chronic sodium depletion and FUROCAP protocols and inhibited the natriorexigenic response induced by sodium depletion in ovariectomized rats. Oestrogen therapy significantly attenuated the losartan-induced antidipsogenic and antinatriorexigenic actions following sodium depletion and FUROCAP protocols. These results indicate that ovariectomized rats express increased AT(1) receptor signalling related to thirst and sodium appetite responses. Oestrogen therapy and brain AT(1) receptor blockade weakened or markedly decreased the behavioural responses during the nocturnal period, a time at which brain angiotensinergic activity is expected to be more prominent. Finally, we demonstrated through different experimental protocols a clear-cut influence of oestrogenic status on the behavioural AT(1)-induced signalling response.

Vasopressin and angiotensin receptors of the medial septal area of the brain in the control of thirst and salt appetite induced by vasopressin in water-deprived and sodium-depleted rats.

In this study we investigated the influence of d(CH(2))(5)-Tyr (Me)-AVP (A(1)AVP) and [Adamanteanacatyl(1),D-ET-D-Tyr(2), Val(4), aminobutyril(6),A(8,9)]-AVP (A(2)AVP), antagonists of V(1) and V(2) arginine(8)-vasopressin (AVP) receptors, respectively, as well as the effects of losartan and CGP42112A, antagonists of angiotensin II (ANGII) AT(1) and AT(2,) receptors, respectively, on water and 0.3 M sodium intake induced by water deprivation or sodium depletion (furosemide treatment) and enhanced by AVP injected into the medial septal area (MSA). A stainless steel cannula was implanted into the medial septal area (MSA) of male Holtzman rats AVP injection enhanced water and sodium intake in a dose-dependent manner. Pretreatment with V(1) antagonist injected into the MSA produced a dose-dependent reduction, whereas prior injection of V(2) antagonist increased, in a dose-dependent manner, the water and sodium responses elicited by the administration of AVP. Both AT(1) and AT(2) antagonists administered into the MSA elicited a concentration-dependent decrease in water and sodium intake induced by AVP, while simultaneous injection of the two antagonists was more effective in decreasing AVP responses. These results also indicate that the increase in water and sodium intake induced by AVP was mediated primarily by MSA AT(1) receptors.

Water deprivation and the double- depletion hypothesis: common neural mechanisms underlie thirst and salt appetite

Water deprivation-induced thirst is explained by the double-depletion hypothesis, which predicts that dehydration of the two major body fluid compartments, the extracellular and intracellular compartments, activates signals that combine centrally to induce water intake. However, sodium appetite is also elicited by water deprivation. In this brief review, we stress the importance of the water-depletion and partial extracellular fluid-repletion protocol which permits the distinction between sodium appetite and thirst. Consistent enhancement or a de novo production of sodium intake induced by deactivation of inhibitory nuclei (e.g., lateral parabrachial nucleus) or hormones (oxytocin, atrial natriuretic peptide), in water-deprived, extracellular-dehydrated or, contrary to tradition, intracellular-dehydrated rats, suggests that sodium appetite and thirst share more mechanisms than previously thought. Water deprivation has physiological and health effects in humans that might be related to the salt craving shown by our species.

Water deprivation and the double- depletion hypothesis: common neural mechanisms underlie thirst and salt appetite.

Water deprivation-induced thirst is explained by the double-depletion hypothesis, which predicts that dehydration of the two major body fluid compartments, the extracellular and intracellular compartments, activates signals that combine centrally to induce water intake. However, sodium appetite is also elicited by water deprivation. In this brief review, we stress the importance of the water-depletion and partial extracellular fluid-repletion protocol which permits the distinction between sodium appetite and thirst. Consistent enhancement or a de novo production of sodium intake induced by deactivation of inhibitory nuclei (e.g., lateral parabrachial nucleus) or hormones (oxytocin, atrial natriuretic peptide), in water-deprived, extracellular-dehydrated or, contrary to tradition, intracellular-dehydrated rats, suggests that sodium appetite and thirst share more mechanisms than previously thought. Water deprivation has physiological and health effects in humans that might be related to the salt craving shown by our species.

Involvement of central H1 and H2 receptors in water intake induced by hyperosmolarity, hypovolemia and central cholinergic stimulation.

In the present study we investigated the participation of central H1 and H2 histaminergic receptors in water intake induced by hyperosmolarity (evoked by intragastric salt load), by hypovolemia (promoted by the subcutaneous administration of polyethyleneglycol) and by the pharmacological stimulation of central cholinergic pathways by the muscarinic agonist carbachol in male Wistar rats. The data presented here show that the pharmacological blockade of central H1 histaminergic receptors by third ventricle injections of mepyramine significantly decreased water intake induced by hyperosmolarity, hypovolemia and by the intracerebroventricular injections of carbachol. On the other hand, the pharmacological blockade of central H2 histaminergic receptors by third ventricle injections of cimetidine significantly reduced water intake in hypovolemic and hyperosmotic animals, but failed to alter water intake induced by central cholinergic stimulation by carbachol. We conclude that H1 and H2 brain histaminergic receptors are involved in inducing thirst during hyperosmolarity and hypovolemia and that H1 histaminergic receptors located post-synaptically in relation to cholinergic pathways seem to be important in triggering drinking following central pharmacological cholinergic stimulation.