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PubMed1980

Transient vasopressin release and thirst in response to prolonged intracerebroventricular infusions of hypertonic mannitol in saline.

In the conscious goat infusions of 0.4 M mannitol in 0.15 M NaCl into the lateral cerebral ventricle (40 or 100 min, 0.02 ml/min) caused slight, transient vasopressin release and temporary thirst, whereas infusions or pure, hypertonic (0.7 M) mannitol did not elicit thirst and inhibited the basic vasopressin release in the nonhydrated animal. In contrast, infusions of equiosmolal (0.35 M) NaCl induced persistent thirst and pronounced elevation of the plasma vasopressin concentration throughout the infusion period. The cerebrospinal fluid (CSF) osmolality was raised by the same order of magnitude (= 13%) after the mannitol/NaCl and the hypertonic NaCl infusions. The CSF Na+ concentration was elevated by greater than 10% at 5 min after hypertonic NaCl infusions, but it was reduced by approximately 10% at 5 min after the mannitol/NaCl infusions. There was no appreciable difference in the CSF K+ concentration after the infusions. The results are discussed with regard to the possible importance of CSF Na+-concentration as opposed to strict osmotic factors for the excitation of receptors involved in the control of water balance.

Animals↗

PubMed1985

Physiological stimuli of thirst and drinking patterns in ponies.

The stimuli that elicit thirst were studied in four ponies. Nineteen hours of water deprivation produced an increase in plasma protein from 67 +/- 0.1 g/litre to 72 +/- 2 g/litre, a mean (+/- se) increase in plasma sodium from 139 +/- 3 to 145 +/- 2 mmol/litre and an increase in plasma osmolality from 297 +/- 1 to 306 +/- 2 mosmol/litre. Undeprived ponies drank 1.5 +/- 0.9 kg/30 mins; 19 h deprived ponies drank 10.2 +/- 2.5 kg/30 mins and corrected the deficits in plasma protein, plasma sodium and plasma osmolality as well as compensating for the water they would have drunk during the deprivation period. In order to determine if an increase in plasma osmolality would stimulate thirst, 250 ml of 15 per cent sodium chloride was infused intravenously. The ponies drank when osmolality increased 3 per cent and when plasma sodium rose from 136 +/- 3 mmol/litre to 143 +/- 3 mmol/litre. Ponies infused with 15 per cent sodium chloride drank 2.9 +/- 0.7 kg; those infused with 0.9 per cent sodium chloride drank 0.7 +/- 0.5 kg. In order to determine if a decrease in plasma volume would stimulate thirst, ponies were injected with 1 or 2 mg/kg bodyweight (bwt) frusemide. Plasma protein rose from 68 +/- 2 g/litre pre-injection to 75 +/- 2 g/litre 1 h after 1 mg/kg bwt frusemide and to 81 +/- 1 g/litre 1 h after 2 mg/kg bwt frusemide.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2003

Drinking behavior and perception of thirst in untrained women during 6 weeks of heat acclimation and outdoor training.

The purposes of this study were to characterize measures of fluid intake and perception of thirst in women over a 6-week period of exercise-heat acclimation and outdoor training and examine if this lengthy acclimation period would result in changes in fluid intake that differ from those previously reported in men utilizing a shorter acclimation protocol of 8-10 days. Voluntary water intake (11-17 degrees C) and perception of thirst were measured in a group of 5 women (21-26 yr) undergoing exercise-heat acclimation for 90 min/day, 3 days/wk (36 degrees C, rh 50-70%) and outdoor training 3 days/wk for 6 weeks. Decreased drinking during acclimation was characterized by a decrease in the number of drinks (35 +/- 10 to 17 +/- 5; p <.05), greater time to first drink (9.9 +/- 2.0 to 23.1 +/- 4.7 min; p <.05), and a decrease in total volume ingested per week (3310 +/- 810 to 1849 +/- 446 ml; p <.05) through the 6-week study. Mean perceived thirst measurements remained low and showed only slight variance (3 +/- 0.4 to 5 +/- 0.4). These observations support a psycho-physiological response pattern different than that previously observed during 8-10 day acclimation protocols in men.

Acclimatization↗

PubMed1978

Mediation of isoproterenol-induced thirst in rats by beta2-adrenergic receptors.

Isoproterenol-induced thirst in rats has been attributed to the activation of beta-adrenergic receptors. Since these receptors can be further differentiated pharmacologically into beta1 and beta2 types, experiments were performed using several beta-adrenergic agonists and antagonists to determine the receptor type initiating the isoproterenol-induced thirst. The beta1- and beta2-adrenergic antagonist, d,l-propranolol (1 mg/kg, ip), blocked the increase in water intake usually accompanying acute subcutaneous administration of isoproterenol (25 microgram/kg) to female rats. Since l-propranolol is known to stabilize membranes and to possess anesthetic-like properties, d-propranolol was also used. This isomer has little beta-adrenergic-blocking activity but possesses anesthetic-like activity. Administration of d-propranolol (1 mg/kg, ip) failed to affect the drinking response to acute administration of isoproterenol (25 microgram/kg). Practolol (125 mg/kg), a beta1-adrenergic antagonist with little anesthetic properties, also had no effect on water intake of isoproterenol-treated rats. Butoxamine, a selective beta2-adrenergic antagonist, attenuated the drinking response to isoproterenol. Salbutamol (150 microgram/kg), a beta2-adrenergic agonist, mimicked the effect of isoproterenol on water intake. These results are consistent with the suggestion that beta2-adrenergic receptors mediate the isoproterenol-induced thirst in rats.

Albuterol↗

PubMed2003

Increased thirst and vasopressin secretion after myocardial infarction in rats.

Impaired regulation of salt and water balance in left ventricular dysfunction and heart failure can lead to pulmonary and peripheral edema and hyponatremia. Previous studies of disordered water regulation in heart failure have used models of low cardiac output with normal cardiac function (e.g., inferior vena cava ligation). We investigated thirst and vasopressin (AVP) secretion in a rat myocardial infarction model of chronic left ventricular dysfunction/heart failure in response to a 24-h water deprivation period. Thirst (implied from water drunk), hematocrit, plasma renin activity, and plasma AVP concentrations increased with water deprivation vs. ad libitum water access. Thirst and plasma AVP concentrations were significantly positively correlated with infarct size after 24-h water deprivation but not under ad libitum water access conditions. The mechanism by which this occurs is unclear but could involve increased osmoreceptor sensitivity, altered stimulation of baroreceptors, the renin-angiotensin system, or altered central neural control.

Animals↗

PubMed2005

Inhibition of thirst when dehydrated rats drink water or saline.

The present experiments sought to identify the physiological signals that inhibit thirst when dehydrated rats drink water or NaCl solution. Rats were deprived of drinking fluid but not food overnight. When allowed to drink again, the dehydrated animals consumed water or saline (0.05 M, 0.10 M, 0.15 M, or 0.20 M NaCl solution) almost continuously for 5-8 min before stopping. The volumes consumed were similar regardless of which fluid they ingested, but blood analyses indicated that increased plasma osmolality and decreased plasma volume, or both, still remained when drinking terminated. These results suggest that the composition of the ingested fluid is less significant than its volume in providing an early signal that inhibits thirst and fluid consumption by dehydrated rats. Analyses of the gastrointestinal tracts revealed that the cumulative volume in the stomach and small intestine correlated highly with the amount consumed regardless of which fluid was ingested. These and other results suggest that the volume of fluid ingested by dehydrated rats is sensed by stretch receptors detecting distension of the stomach and small intestine, which provide an early inhibitory stimulus of thirst.

Animals↗

PubMed1977

Preoptic-hypothalamic periventricular lesions: thirst deficits and hypernatremia.

To assess the significance of stimulation studies suggesting an anteroventral third ventricle (AV3V) dipsogenic site of action for hyperosmotic and angiotensin thirst stimuli, electrolytic lesions of periventricular tissue surrounding AV3V were produced under ether anesthesia in rats preselected for responsiveness to subcutaneous angiotensin and hypertonic NaCl thirst challenges. Lesions limited to preoptic-anterior hypothalamic periventricular substrates resulted in adipsia; those rats resuming ad lib. drinking after a period of adipsia exhibited persistent drinking deficits to angiotensin and hypertonic NaCl thirst challenges, reduced drinking after water deprivation, and increased plasma osmolality and sodium. Drinking to polyethylene glycol-induced hypovolemia and feeding after food deprivation did not differ between lesioned and sham-lesioned animals. The disturbances in behavioral control of fluid balance imply that AV3V periventricular tissue normally plays a key role in mediating regulatory drinking. It is proposed that these AV3V periventricular lesion-induced effects on drinking behavior are due to destruction of receptors and/or integrative systems monitoring fluid-borne angiotensin and hyperosmotic stimuli.

Angiotensin II↗

PubMed1979

Inhibition of osmotic thirst by electric stimulation of the basal forebrain in dogs.

The effect of electrical brain stimulation (ESB; 50 Hz, 50-150 microA sine wave, 5 s on/5 s off) on osmotic thirst was examined in 10 conscious dogs chronically implanted with electrodes aimed at the anteromedial part of the basal forebrain. Suppression of osmotic thirst (SOT) was observed during stimulation through 18 of 41 electrodes located in the olfactory tubercle, the nucleus accumbens, the caudate nucleus, the medial septum, and the lateral preoptic-anterolateral hypothalamic area (PrA/ALH). Mean increment in plasma osmolality necessary to cause drinking rose from 9.0 +/- 1.5 mosmol (X +/- SE; n = 15) under control conditions to 15.8 +/- 2.6 mosmol (n = 18) during ESB in SOT placements. Threshold cellular dehydration eliciting drinking increased from 2.70 +/- 0.50% of intracellular water (ICW;n = 16) to 4.77 +/- 0.68% of ICW (n = 18), respectively. The strongest SOT was found during ESB in the nucleus accumbens, and the PrA/ALH. The same stimulation failed to inhibit feeding, support self-stimulation or produce appreciable changes of dog's gross behavior. The results give evidence for the existence in the basal forebrain of the dog a widely distributed neural system suppressing osmotic thirst. The nucleus accumbens and the PrA/ALH seem to play an important role in this system.

Animals↗

PubMed1982

Physiological mechanisms for thirst in the nonhuman primate.

The relationship between body fluid deficits and drinking has been investigated in a nonhuman primate. Intravenous sodium chloride infusions (0.93-3.25 M) given to rhesus monkeys caused drinking correlated with increases in plasma osmolality and sodium concentrations. Sucrose infusions (0.3 M in 0.15 M NaCl) also caused drinking while equiosmolal urea infusions did not. It was found that the drinking threshold corresponded to a 2.3% increase in plasma osmolality. Water deprivation for 24 h caused significant cellular dehydration, as indicated by a 5.8% elevation in plasma osmolality that exceeded the threshold for thirst, and a significant hypovolemia as indicated by elevated plasma protein and hematocrit values. Intravenous water preloads decreased plasma osmolality and produced a dose-related decrease in subsequent drinking. Infusions that restored plasma osmolality to predeprivation values, reduced intake by 85%. Intravenous isotonic saline preloads which abolished the hypovolemia did not have a consistent effect and reduced mean water intakes by only 3.2%. Thus in the rhesus monkey, cellular dehydration is an effective stimulus for thirst, and it is the primary determinant of drinking after water deprivation, used as an example of a natural thirst stimulus. In contrast to findings in nonprimates, the extracellular deficit contributes very little to drinking after water deprivation.

Animals↗

PubMed1995

Mechanism of thirst attenuation during head-out water immersion in men.

The purpose was to determine whether extracellular volume or osmolality was the major contributing factor for reduction of thirst in air and head-out water immersion in hypohydrated subjects. Eight males (19-25 yr) were subjected to thermoneutral immersion and thermoneutral air under two hydration conditions without further drinking: euhydration in water (Eu-H2O) and euhydration in air, and hypohydration in water (Hypo-H2O) and hypohydration in air (3.7% wt loss after exercise in heat). The increased thirst sensation with Hypo-H2O decreased (P < 0.05) within 10 min of immersion and continued thereafter. Mean plasma osmolality (288 +/- 1 mosmol/kgH2O) and sodium (140 +/- 1 meq/l) remained elevated, and plasma volume increased by 4.2 +/- 1.0% (P < 0.05) throughout Hypo-H2O. A sustained increase (P < 0.05) in stroke volume accompanied the prompt and sustained decrease in plasma renin activity and sustained increase (P < 0.05) in plasma atrial natriuretic peptide during Eu-H2O and Hypo-H2O. Plasma vasopressin decreased from 5.3 +/- 0.7 to 2.9 +/- 0.5 pg/ml (P < 0.05) during Hypo-H2O but was unchanged in Eu-H2O. These findings suggest a sustained stimulation of the atrial baroreceptors and reduction of a dipsogenic stimulus without major alterations of extracellular osmolality in Hypo-H2O. Thus it appears that vascular volume-induced stimuli of cardiopulmonary baroreceptors play a more important role than extracellular osmolality in reducing thirst sensations during immersion in hypohydrated subjects.

Adult↗

PubMed1978

Field dependence and the effect of REM deprivation on thirst.

Recently a number of studies have concerned the possible function of rapid eye movement (REM) sleep and the mastery of stress. The present study was designed to explore the possibility that REM sleep might play a function in reducing the potency of a stressful physiological stimulus, thirst, as well as the possibility that such a function might be specific to individuals falling at different points along the field-dependence dimension. While there was no difference between REM deprivation and non-REM awakening nights in subsequent morning thirst, there was a significant interaction between field dependence and night on morning thirst measures for 10 college students. These results are discussed in light of previous work on stylistic differences in dreaming and their possible role in adaptation to stress.

Adaptation, Physiological↗

PubMed1978

Osmotic thirst suppression elicited by electrical stimulation of the basal forebrain in the dog.

Reactivity of the thirst mechanism to osmotic stimuli was measured in conscious dogs chronically implanted with electrodes in the basal forebrain. It was found that the thirst threshold to the osmotic stimulus increases markedly during electrical stimulation of the preoptic area, septum, nucleus accumbens septi, and to smaller degree during stimulation of the nucleus caudatus. The possibility of existence of some inhibitory components in the neural system controlling thirst in the dog is suggested.

Animals↗

PubMed1978

Central neural pathways for angiotensin-induced thirst.

Evidence is reviewed implicating the preoptic region in angiotensin-induced thirst. The most responsive area according to results obtained with behavioral, electrophysiological, and autoradiographic mapping techniques is at the caudal border of the medial preoptic region and rostral border of the anterior hypothalamus. The neural pathway from this preoptic site for angiotensin-induced thirst extends along the medial forebrain bundle through the midlateral hypothalamus to the paramedial midbrain tegmentum and to an area ventrolateral to the central gray. Lesions of this pathway in the midlateral hypothalamus and rostral midbrain significantly attenuated drinking induced by microinjections of angiotensin II into the preoptic area but did not disrupt water intake induced by microinjections of angiotensin II into the subfornical organ or cerebral ventricles. Although the efferent pathways from angiotensin-receptive sites in the subfornical organ and cerebral ventricles are unknown, it appears from these observations that the medial forebrain bundle is not involved. Lesions of the medial forebrain bundle-lateral hypothalamus also do not disrupt drinking induced by microinjections of hypertonic saline into the preoptic region although lesions placed 1 mm further lateral do. Since fat lateral hypothalamic lesions are without effect on drinking induced by centrally administered angiotensin II, this suggests that intracellular and extracellular thirst signals are subserved by separate neural pathways in the hypothalamus.

Action Potentials↗

PubMedDate not supplied

Thirst: a critical care nursing challenge.

Thirst is a symptom commonly experienced by critically ill patients. Critical care nurses have the opportunity to prevent and reduce thirst by recognizing the types of thirst, identifying patients at risk, monitoring physiological parameters, and providing comfort measures.

Adolescent↗

PubMedDate not supplied

[Electrophysiologic analysis of the conditioned reflex activity of cats against a background of thirst].

EEG of the cerebral cortex and hypothalamic electrogram of cats during salt load and water deprivation were recorded at performance of conditioned running elicited by signals of insipid and salt food. The signal of insipid food presented during thirst was accompanied only by the cerebral cortex activation, while the salt signal involved in activation not only the cortex but the hypothalamus as well. In cases when the insipid signal was reinforced by salt food and the animal ate it (though during thirst it rejected the food), strong cortex activation was observed with the involvement of paraventricular parts of the hypothalamus. During intense thirst reversal was obtained of the signal role of the conditioned cue in accordance with the new quality of the alimentary reinforcement. Hypothalamo-cortical mechanisms of dominant motivation and its conditioned provision are discussed.

Animals↗

PubMed1988

Lesions in the mesencephalic reticular formation change open field and thirst motivated labyrinth behaviour of rats.

Open field behaviour and thirst motivated running through two labyrinth variants were compared before and after bilateral symmetric lesions of the anterior part of the dorsolateral parabrachial nucleus (PBl) and in the anterior mesencephalic area cuneiformis (CU), both n = 9, on 4-month-old male Long-Evans rats. CU-rats were characterized by abolished visual placing responses, aphagia or hypophagia which was limited up to the 15th postoperative day, ambulatory hyperactivity, reduced climbing and grooming, but enhanced rearing. Their preoperatively learnt thirst motivated labyrinth passage remained unimpaired but their drinking behaviour was persistently changed. They interrupted drinking several times and regularly did not empty the cups. Thirst motivation was evidently reduced after CU-lesions. PBl-rats were ambulatory hypoactive and slowed with accelerated habituation, reduced climbing and changed incline-plane behaviour. A slight hypophagia was generally overcome after the 5th postoperative day. Labyrinth performance of PBl-rats was evidently changed with significantly slower runs and impaired differentiation of the second labyrinth type in which passage duration, errors and even duration of licking were enhanced. Water intake was less reduced than in CU-rats. Both nuclei include parts of the "mesencephalic locomotor region", but contribute differently to the regulation of spontaneous and goal-directed behaviour.

Animals↗

PubMed1995

Inhibition of nitric oxide synthase attenuates osmotic thirst in the rat.

Changes in water intake after intraperitoneal injection of a nitric oxide synthase (NOS) inhibitor was studied in the rat. Administration of NW-nitro-L arginine methyl ester (L-NAME) at a dose of 50 mg/kg attenuated osmotic thirst induced by intraperitoneal injection of hypertonic saline, but did not affect spontaneous intake of water and thirst induced by subcutaneous injection of angiotension II. Pretreatment with L-arginine significantly attenuated the inhibition of osmotic thirst evoked with subsequent L-NAME. Administration of NW-nitro-D-arginine methyl ester (D-NAME) altered neither the spontaneous nor the osmotic drinking behavior. These findings suggest that NO may affect the osmotically induced drinking.

Angiotensin II↗

PubMed2000

Effects of dehydration on plasma osmolality, thirst-related behavior, and plasma and brain angiotensin concentrations in Couch's spadefoot toad, Scaphiopus couchii.

Under dehydrating conditions, many terrestrial vertebrates species exhibit increases in plasma osmolality and their drinking behavior. Under some circumstances, this behavioral change is accompanied by changes in plasma and central angiotensin concentrations, and it has been proposed that these changes in angiotensin levels induce the thirst-related behaviors. In response to dehydration, the spadefoot toad, Scaphiopus couchii, exhibits thirst-related behavior in the form of cutaneous drinking. This behavior has been termed water absorption response (WR) behavior. Spadefoot toads live in harsh desert environments and are subject annually to dehydrating conditions that may induce thirst-related behavior. We tested the hypothesis that an increase in WR behavior is associated with both an increase in plasma osmolality and an increase in plasma and brain angiotensin concentrations. First, we determined the degree of dehydration that was necessary to initiate WR behavior. Animals dehydrated to 85% of their standard bladder-empty weight via deprivation of water exhibited WR behavior more frequently than control toads left in home containers with water available. Next, using the same dehydration methods, we determined the plasma osmolality and sodium concentrations of dehydrated toads. Toads dehydrated to 85% standard weight also had a significant increase in plasma osmolality, but exhibited no overall change in plasma sodium concentrations, indicating that while an overall increase in plasma osmolality appears to be associated with WR behavior in S. couchii, changes in sodium concentrations alone are not sufficient to induce the behavior. Finally, plasma and brain angiotensin concentrations were measured in control toads and toads dehydrated to 85% standard weight. Plasma and brain angiotensin concentrations did not increase in dehydrated toads, indicating that dehydration-induced WR behavior that is associated with changes in plasma osmolality may not be induced by changes in endogenous angiotensin concentrations in S. couchii.

Angiotensin II↗