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Physiology of thirst and drinking: implication for nursing practice.

Thirst and drinking function to maintain body water balance and are basic to survival. Thirst is often associated with a dry unpleasant-tasting mouth and the feeling of a need to obtain water; it can result from dehydration, decreased vascular volume, dry mouth, pharmacologic agents, or inappropriate activation of the thirst mechanism. Drinking involves the motor activities that culminate in ingestion of liquids. Thirst sensation and drinking are influenced by many factors, including the temperature and taste of a liquid. Thirst may be discomforting in persons with limited fluid intake, diminished in some elderly persons, and inappropriate in persons who are compulsive water drinkers. Although nurses are commonly confronted with client complaints of thirst, there has been minimal nursing research that relates to assessment of thirst and drinking behaviors, nursing diagnoses for thirst, or nursing interventions for persons with altered thirst or drinking behaviors.

Compulsive Behavior↗

Thirst in diabetes insipidus: clinical relevance of quantitative assessment.

Patients with cranial diabetes insipidus are unable to concentrate urine, and depend on thirst and water intake to prevent hypertonic dehydration. Using a visual analogue scale (0-10 cm) we studied osmotically stimulated thirst induced by hypertonic saline infusion in 15 patients with diabetes insipidus and 15 healthy controls. Plasma osmolality in the patients rose from 292 +/- 1 to 316 +/- 1 mOsm/kg (p less than 0.001), and 13 patients showed a progressive rise in thirst ratings (1.4 +/- 0.4 to 8.1 +/- 0.3 cm, p less than 0.001) with abolition of thirst by drinking, in a similar fashion to controls. Water intake following infusion was greater in patients than controls (p less than 0.001). Linear regression analysis of thirst and plasma osmolality showed no difference in the osmotic threshold for thirst onset, or the sensitivity of thirst osmoreceptors, between 13 of the patients and the control group. One patient was shown to be hypodipsic and compulsive water drinking was demonstrated in another: abnormal thirst perception caused abnormalities of salt and water balance in these two patients. Most patients with cranial diabetes insipidus have normal thirst mechanisms, though clinically significant hypodipsia or hyperdipsia may co-exist with vasopressin deficiency.

Adult↗

Dipsogenic diabetes insipidus: a newly recognized syndrome caused by a selective defect in the osmoregulation of thirst.

We describe three patients who have polydipsia and polyuria due to an abnormality in the osmoregulation of thirst. The clinical manifestations of the syndrome are similar to those of neurogenic diabetes insipidus. Thus, under basal conditions the patients have thirst, normal to high normal levels of plasma osmolality, and low levels of plasma vasopressin. Moreover, antidiuretic therapy greatly reduces thirst and polydipsia as well as polyuria. The only clinically distinguishing feature of the response is that thirst and water intake decrease less rapidly than water excretion. As a consequence, the patients with this syndrome develop variable degrees of dilutional hyponatremia and hypoosmolemia during treatment. The plasma vasopressin response to osmotic stimulation is relatively normal. In most of the patients, the osmotic threshold for vasopressin release is at the upper limit of normal, but this finding only explains their modest elevation in basal plasma osmolality. Thirst and water intake also change as a function of plasma osmolality. However, the threshold or "set" of the thirst osmostat appears to be abnormally low. The degree of downward resetting varies from patient to patient, but is always sufficient to stimulate thirst and water intake at levels of plasma osmolality below the normal range. This abnormality can account not only for the thirst and polyuria under basal conditions but also for the overhydration that occurs during antidiuretic therapy. The pathogenesis of the osmoregulatory abnormality is unknown but may be due to disruption of one or more of the afferent pathways that regulate the "set" of the thirst and vasopressin osmostats.

Adult↗

The importance of thirst in maintenance of fluid balance.

Plasma osmolality is maintained within very narrow limits by the control of water intake via thirst and water output via secretion of vasopressin. Osmoreceptors are situated in the brain, but on the blood side of the blood-brain barrier in a circumventricular organ. These regions are stimulated by an increase in plasma osmolality and form the most important input to cause thirst and drinking. Cardiopulmonary and arterial baroreceptors sensitive to blood volume and blood pressure also can be important, so hypovolaemic events such as haemorrhage can stimulate thirst. Both raised plasma osmolality and reduced blood volume contribute to thirst and vasopressin secretion following water deprivation. The importance of the nucleus medianus in the neural circuitary involved in integrating thirst should be emphasized. Mechanisms which stop drinking are different from those which initiate it, and oropharyngeal metering of the volume of fluid consumed provides the important input. There are a number of situations in humans where thirst thresholds and sensitivities are altered. The elderly have higher thirst thresholds and this can cause symptoms of dehydration. Increased drinking is seen in congestive heart failure, renal hypertension and certain cerebral lesions. Thirst thresholds are set at lower levels in pregnancy and in the luteal phase of the menstrual cycle and may contribute to fluid retention in these situations.

Aging↗

Osmoregulation of thirst and vasopressin release in severe chronic renal failure.

Subjects with severe chronic renal failure (CRF) have higher plasma concentrations of arginine vasopressin (AVP) than normal subjects, and some develop severe thirst. Eight patients with CRF and seven matched controls underwent hypertonic saline infusion to explore the relationship of thirst and plasma AVP with plasma osmolality. Differences in urea concentration between the two groups were controlled for by correcting measured osmolality to a urea of zero. Linear regression analysis of the relationships between plasma AVP and thirst with plasma osmolality (corrected for urea) was performed. Mean results were: control, pAVP = 0.26 (pOsmc - 283.7) versus CRF, pAVP = 0.72 (pOsmc - 282.0); and control, thirst = 4.0 (pOsmc - 279.4) versus CRF, thirst = 3.5 (pOsmc - 281.8). The apparent sensitivity (slope) of AVP release was greater in severe CRF than in normal controls (P = 0.04). There was no significant difference between the groups in thirst sensitivity, threshold for thirst onset and threshold for AVP release. Osmoregulated thirst was normal in severe CRF, but increasing osmolality leads to higher concentrations of AVP than would be expected.

Adult↗

Neural correlates of the emergence of consciousness of thirst.

Thirst was induced by rapid i.v. infusion of hypertonic saline (0.51 M at 13.4 ml/min). Ten humans were neuroimaged by positron-emission tomography (PET) and four by functional MRI (fMRI). PET images were made 25 min after beginning infusion, when the sensation of thirst began to enter the stream of consciousness. The fMRI images were made when the maximum rate of increase of thirst occurred. The PET results showed regional cerebral blood flow changes similar to those delineated when thirst was maximal. These loci involved the phylogenetically ancient areas of the brain. fMRI showed activation in the anterior wall of the third ventricle, an area that is key in the genesis of thirst but is not an area revealed by PET imaging. Thus, this region plays as major a role in thirst for humans as for animals. Strong activations in the brain with fMRI included the anterior cingulate, parahippocampal gyrus, inferior and middle frontal gyri, insula, and cerebellum. When the subjects drank water to satiation, thirst declined immediately to baseline. A precipitate decline in intensity of activation signal occurred in the anterior cingulate area (Brodmann area 32) putatively related to consciousness of thirst. The intensity of activation in the anterior wall of the third ventricle was essentially unchanged, which is consistent with the fact that a significant time (15-20 min) would be needed before plasma Na concentration changed as a result of water absorption from the gut.

Adult↗

Sodium balance modulates thirst in normal man.

Several lines of evidence suggest that angiotensin II (AII) plays an important physiologic role in the control of thirst in laboratory animals but a conflicting one in humans. Sodium (Na+) balance plays a key role in the control of the renin-angiotensin system, but studies assessing the effect of sodium balance on thirst perception in humans are limited at best. To address this question, we studied the relationship between thirst perception and plasma osmolality during 5% saline infusion (.08 ml/kg/min x 120 min) in 5 healthy volunteers while in metabolic balance on both a 10 mEq. sodium (LS) and 200 mEq. sodium (HS) diet with and without infusion of AII (5 ng/kg/min). Thirst perception was quantified using a linear visual analogue scale. The relationship between serum Na+ (a measure of osmolality) and thirst perception was analyzed using linear regression. The mean x-intercept ([Na+] mEq/l) which represents the osmotic threshold to thirst was 138.2 +/- 0.5 in LS vs 140.7 +/- 0.8 in HS, p < 0.05. We conclude that the osmotic threshold for thirst is lower in LS (high endogenous AII) vs HS (low endogenous AII). There was no evidence for substantial extracellular volume change in HS vs LS with no significant differences in weight, hematocrit or total serum protein. Acute AII infusion did not result in changes in slope or x-intercept, but the pressor response to exogenous AII may have inhibited its dipsogenic effect (as has been shown in animal studies). These data suggest a physiologic role of sodium balance (possibly mediated via endogenous AII) in the control of thirst in normal humans.

Aldosterone↗

Thirst distress and interdialytic weight gain: how do they relate?

Thirst is a frequent and stressful symptom experienced by hemodialysis patients. Several studies have noted a positive relationship between thirst and interdialytic weight gain (IDWG). These factors prompted us to consider ways that we could intervene to reduce thirst and IDWG through an educative, supportive nursing intervention. This paper presents the results of a pilot research project, the purpose of which was to: examine the relationship between thirst distress (the negative symptoms associated with thirst) and IDWG in a sample of our patients, describe patients' strategies for management of thirst, and establish the necessary sample size for the planned intervention study. The pilot research project results showed that in a small sample of 20, there was a mildly positive, though not statistically significant, correlation between thirst distress and IDWG (r = 0.117). Subjects shared a wide variety of thirst management strategies including: limiting salt intake, using ice chips, measuring daily allotment, performing mouth care, eating raw fruits and vegetables, sucking on hard candy and chewing gum. This pilot research project showed that given an alpha of 0.05 and a power of 80%, we will require a sample of 39 subjects to detect a 20% change in IDWG. We will employ these results to plan our intervention study, first by establishing the appropriate sample size and second by incorporating identified patient strategies into an educational pamphlet that will form the basis of our intervention.

Adaptation, Psychological↗

Physiological and pathophysiological influences on thirst.

Thirst motivates animals to seek fluid and drink it. It is regulated by the central nervous system and arises from neural and chemical signals from the periphery interacting in the brain to stimulate a drive to drink. Our research has focussed on the lamina terminalis and the manner in which osmotic and hormonal stimuli from the circulation are detected by neurons in this region and how that information is integrated with other neural signals to generate thirst. Our studies of osmoregulatory drinking in the sheep and rat have produced evidence that osmoreceptors for thirst exist in the dorsal cap of the organum vasculosum of the lamina terminalis (OVLT) and in the periphery of the subfornical organ, and possibly also in the median preoptic nucleus. In the rat, the hormones angiotensin II and relaxin act on neurons in the periphery of the subfornical organ to stimulate drinking. Studies of human thirst using functional magnetic resonance imaging (fMRI) techniques show that systemic hypertonicity activates the lamina terminalis and the anterior cingulate cortex, but the neural circuitry that connects sensors in the lamina terminalis to cortical regions subserving thirst remains to be determined. Regarding pathophysiological influences on thirst mechanisms, both excessive (polydipsia) and inadequate (hypodisia) water intake may have dire consequences. One of the most common primary polydipsias is that observed in some cases of schizophrenia. The neural mechanisms causing the excessive water intake in this disorder are unknown, so too are the factors that result in impaired thirst and inadequate fluid intake in some elderly humans.

Animals↗

Controls of vasopressin secretion and thirst: similarities and dissimilarities in signals.

RATS HAVE TWO PROMINENT RESPONSES TO DEHYDRATION: secretion of the antidiuretic hormone, vasopressin (VP), and thirst. Many signals directly affect both responses. These include two excitatory signals associated with increased plasma osmolality (pOsm) and two inhibitory signals associated with decreased pOsm (one each from cerebral and visceral osmoreceptors). In addition, both VP secretion and thirst during hypovolemia are stimulated by at least two signals, one neural (from cardiac baroreceptors) and one humoral (i.e., angiotensin II). In contrast to these evident similarities, there are definite dissimilarities in the signals for VP secretion and thirst. For example, acute hypervolemia inhibits VP secretion but not thirst, whereas acute hypertension inhibits thirst but not VP secretion. Thirst and VP secretion in rats each are stimulated by acute arterial hypotension, albeit not by the same signals; water intake is mediated by activation of the renin-angiotensin system but not by a neural signal from arterial baroreceptors, whereas the reverse may be true for the stimulation of VP secretion. These dissimilarities indicate that VP secretion and thirst in rats are neither invariably linked nor controlled by the same mechanisms.

Animals↗

Neuroimaging evidence implicating cerebellum in support of sensory/cognitive processes associated with thirst.

Recent studies implicate the cerebellum, long considered strictly a motor control structure, in cognitive, sensory, and affective phenomenon. The cerebellum, a phylogenetically ancient structure, has reciprocal ancient connections to the hypothalamus, a structure important in vegetative functions. The present study investigated whether the cerebellum was involved in vegetative functions and the primal emotions engendered by them. Using positron emission tomography, we examined the effects on the cerebellum of the rise of plasma sodium concentration and the emergence of thirst in 10 healthy adults. The correlation of regional cerebral blood flow with subjects' ratings of thirst showed major activation in the vermal central lobule. During the development of thirst, the anterior and posterior quadrangular lobule, lingula, and the vermis were activated. At maximum thirst and then during irrigation of the mouth with water to alleviate dryness, the cerebellum was less activated. However, 3 min after drinking to satiation, the anterior quadrangular lobule and posterior cerebellum were highly activated. The increased cerebellar activity was not related to motor behavior as this did not occur. Instead, responses in ancient cerebellar regions (vermis, fastigal nucleus, archicerebellum) may be more directly related to vegetative and affective aspects of thirst experiences, whereas activity in neocerebellar (posterior) regions may be related to sensory and cognitive aspects. Moreover, the cerebellum is apparently not involved in the computation of thirst per se but rather is activated during changes in thirst/satiation state when the brain is "vigilant" and is monitoring its sensory systems. Some neocerebellar activity may also reflect an intentionality for gratification by drinking inherent in the consciousness of thirst.

Adult↗

Low sodium haemodialysis reduces interdialytic fluid consumption but paradoxically increases post-dialysis thirst.

BACKGROUND: Interdialytic weight gain (IDWG) can be reduced by lowering the dialysate sodium concentration ([Na]) in haemodialysis patients. It has been assumed that this is because thirst is reduced, although this has been difficult to prove. We compared thirst patterns in stable haemodialysis patients with high and low IDWG using a novel technique and compared the effect of low sodium dialysis (LSD) with normal sodium dialysis (NSD). METHODS: Eight patients with initial high IDWG and seven with low IDWG completed hourly visual analogue ratings of thirst using a modified palmtop computer during the dialysis day and the interdialytic day. The dialysate [Na] was progressively reduced by up to 5 mmol/l over five treatments. Dialysis continued at the lowest attained [Na] for 2 weeks and the measurements were repeated. The dialysate [Na] then returned to baseline and the process was repeated. RESULTS: Baseline interdialytic day mean thirst was higher than the dialysis day mean for the high IDWG group (49.9+/-14.0 vs 36.2+/-16.6) and higher than the low weight gain group (49.9+/-14.0 vs 34.1+/-14.6). This trend persisted on LSD, but there was a pronounced increase in post-dialysis thirst scores for both groups (high IDWG: 46+/-13 vs 30+/-21; low IDWG: 48+/-24 vs 33+/-18). The high IDWG group demonstrated lower IDWG during LSD than NSD (2.23+/-0.98 vs 2.86+/-0.38 kg; P<0.05). CONCLUSIONS: Our results indicate that patients with high IDWG experience more intense feelings of thirst on the interdialytic day. LSD reduces their IDWG, but paradoxically increases thirst in the immediate post-dialysis period.

Drinking↗

Influence of age on thirst and fluid intake.

Independently living older adults (over the age of 65 yr) consume adequate volumes of fluids on a daily basis. However, when challenged by fluid deprivation, a hyperosmotic stimulus, or exercise in a warm environment (all of which combine hypovolemia and hyperosmolality), older adults exhibit decreased thirst sensation and reduced fluid intake. Full fluid restoration eventually occurs, but full restoration of fluid balance is slowed. The aging process alters important physiological control systems associated with thirst and satiety. Recent evidence suggests that older men and women (i) have a higher baseline osmolality and thus a higher osmotic operating point for thirst sensation (with little or no change in sensitivity), and (ii) exhibit diminished thirst and satiety in response to the unloading (hypovolemia) and loading (hypervolemia) of baroreceptors. A diminished sensation of thirst in the elderly relative to young adults is generally absent when a volume stimulus is absent, despite higher baseline plasma osmolalities. Compared with the elderly, there are scant data associated with homeostatic control of thirst in children. Nonhomeostatic control of thirst and drinking behavior may likewise be different for children (as it is for the elderly), as compared with young adults; however, little empirical data exist on this topic. Children rarely exhibit voluntary dehydration for activities lasting 45 min or less; however, drink flavoring and sodium chloride are important promoters of drinking in active children.

Adolescent↗

Disturbance of osmoregulated thirst and vasopressin secretion in thyrotoxicosis.

OBJECTIVE: To assess the effect of untreated thyrotoxicosis on osmoregulated thirst sensation and AVP secretion. DESIGN: Measurements were made at 30-minute intervals while untreated thyrotoxic patients were given sodium chloride 855 mmol/l intravenously for 2 hours followed by water drinking ad libitum for 2 hours. The protocol was repeated when the patients were euthyroid. PATIENTS: Eight newly diagnosed thyrotoxic patients were studied. MEASUREMENTS: Thirst sensation (visual analogue scale), plasma osmolality, AVP and plasma renin activity were measured. RESULTS: Prior to osmotic stimulation and after plasma osmolality had been returned to normal by drinking water, thirst sensation was increased in the thyrotoxic state. Plasma AVP showed an exaggerated response to hypertonic saline in the patients when they were thyrotoxic. Increasing plasma osmolality produced a linear increase in thirst sensation and log linear increase in plasma AVP. However, in the thyrotoxic state both these relations were altered. The apparent osmolar thresholds for onset of thirst sensation and AVP release were similar (281 and 280 mosm/kg respectively) and were reduced similarly in the thyrotoxic state (269 and 274 mosm/kg respectively). CONCLUSIONS: The osmostat mechanisms which regulate thirst sensation and AVP release are reset in the thyrotoxic state. The responses of thirst sensation and of plasma AVP to increasing plasma osmolality are altered similarly, suggesting that thyrotoxicosis affects both homeostatic functions by a common mechanism.

Adult↗

Osmoregulation of vasopressin and thirst: comparison of 20% mannitol with 5% saline as osmotic stimulants in healthy man.

OBJECTIVE: Osmoregulation is normally studied using a 5% saline infusion. This may be deleterious in fluid overloaded patients. Twenty per cent mannitol is another osmotic stimulant. This study aimed to compare 20% mannitol infusion with 5% saline as an osmotic stimulant to thirst and vasopressin secretion in normal volunteers. DESIGN AND PATIENTS: Eight healthy volunteers studied on 2 occasions in random order. Each study involved a 2-hour infusion period of either hypertonic (5%) saline (0.06 ml/kg/h) or hypertonic (20%) mannitol (0.07 ml/kg/h). MEASUREMENTS: Plasma vasopressin (pVp), plasma sodium, plasma osmolality (pOsm), haematocrit (HCT), blood pressure, thirst, blood glucose and volume drunk at end of infusion. RESULTS: Five per cent saline infusion stimulated significantly higher levels of pOsm, pVp and thirst than 20% mannitol. Plasma sodium rose significantly during 5% saline infusion and fell during 20% mannitol infusion. HCT fell and mean arterial pressure rose in both infusions but the changes were not clinically significant. Piecewise linear regression analysis defined the overall threshold for pVp release for the two solutions as 5% saline, 292 mosm/kg and 20% mannitol, 291 mosm/kg, and the post threshold slope as 5% saline, 0.46 pmol/l pVp per mosm and 20% mannitol, 0.30 pmol/l pVp per mosm. The threshold for thirst onset was 5% saline, 291 mosm/kg and 20% mannitol, 290 mosm/kg, and the post threshold slope, 5% saline, 0.58 cm thirst per mosm and 20% mannitol, 0.28 cm thirst per mosm. The differences between the calculated osmotic thresholds and slopes post threshold for the two infusions were not significant for the pVp versus pOsm relationship. The difference between the cumulative volume drunk following the two infusions did not reach statistical significance. Mannitol caused a significant diuresis. CONCLUSIONS: Twenty per cent mannitol infusion is an effective osmotic stimulant to thirst and vasopressin release in normal individuals, but is less potent than 5% saline infusion.

Adult↗

Assessment of residual gastric volume and thirst in patients who drink before gastroscopy.

BACKGROUND: Before endoscopy patients undergo an uncomfortable fluid fast to reduce the risk of gastric acid aspiration and to ensure good endoscopic views are obtained. However, fluids rapidly leave the stomach and thus a long fluid fast before endoscopy may not be required. AIMS: The object of this study was to establish whether drinking before endoscopy is safe and relieves patients' symptoms of thirst. PATIENTS AND METHODS: 88 patients with American Society of Anaesthesiologists classification of physical status grades I and II were recruited in a controlled randomised single blind trial. The volume and pH of gastric aspirate obtained at gastroscopy was assessed in patients who drank 330 ml of water a minimum 90 minutes before their endoscopy and compared with values in patients who starved overnight. RESULTS: 44 patients who drank ('drinkers') 330 ml of water a mean 117 minutes before their morning gastroscopy had a similar volume and pH of gastric aspirate compared with 44 patients starved overnight ('starvers'); median volume 12.5 ml versus 10 ml, median pH 2.0 versus 2.0; 'drinkers' versus 'starvers' (NS). Before endoscopy patients were asked to score their thirst and hunger ratings as either none, mild, moderate or severe. Ratings for moderate and severe thirst were grouped together for analysis. The percentage of drinkers compared with starvers in each group with no thirst, mild thirst, and moderate severe thirst was 63%, 46%, and 37% respectively (chi 2 test for trend p < 0.05). Hunger ratings were similar in the two groups. CONCLUSIONS: It is safe for elective day cases to drink a significant volume of water two hours before endoscopy and this alleviates symptoms of thirst.

Adult↗

Effects of ethanol ingestion on thirst and fluid consumption in humans.

To investigate the effects of ethanol on thirst, fluid intake was measured in 24 normal subjects for 3 h after consumption of 1.0 g/kg ethanol, with or without administration of a vasopressin analogue (DDAVP) before ethanol ingestion. Fluid consumption was reduced in subjects receiving DDAVP, suggesting that thirst after ethanol is largely secondary to dehydration due to inhibition of vasopressin release. Further, the effects of ethanol on salt-load-elicited thirst and fluid consumption in normal subjects were studied using intravenous hypertonic saline infusions. Subjects acted as their own controls and received 0.5 or 1.0 ml/kg ethanol 30 min before infusions on one day and an equal volume of fluid on another day. During infusions after ethanol, subjects experienced thirst later and at higher osmolalities. They also drank less immediately after infusions with prior ethanol ingestion. The relationship between thirst score and plasma osmolality was shifted to higher osmolalities by ethanol. Thus, although ethanol progressively causes thirst secondary to dehydration, it has a direct inhibitory effect on the thirst response to osmotic stimulation.

Deamino Arginine Vasopressin↗

Acute suppression of plasma vasopressin and thirst after drinking in hypernatremic humans.

Drinking rapidly abolishes thirst and vasopressin secretion in dehydrated humans before major changes in plasma osmolality are observed. We studied the effects of drinking on plasma vasopressin and thirst in seven healthy volunteers rendered hypernatremic by the infusion of hypertonic (855 mmol/l) sodium chloride solution. Thirst was measured on a visual analogue scale (0-10 cm). Infusion of hypertonic saline caused linear increases in plasma osmolality (289 +/- 1 to 306 +/- 1 mosmol/kg, mean +/- SE, P less than 0.001), plasma vasopressin (0.6 +/- 0.2 to 6.4 +/- 1.9 pmol/l, P less than 0.001), and thirst (1.4 +/- 0.4 to 7.4 +/- 0.5 cm, P less than 0.001). Water was allowed 15 min after cessation of the infusion, and within 5 min of drinking both plasma vasopressin and thirst were significantly lower than postinfusion. After 20 min of drinking, plasma vasopressin had fallen from 6.5 +/- 0.9 to 1.3 +/- 0.3 pmol/l (P less than 0.001) and thirst from 7.7 +/- 0.5 to 1.0 +/- 0.2 cm (P less than 0.001) despite no significant change in plasma osmolality (306 +/- 0.9 to 304 +/- 0.8 mosmol/kg, P = 0.17), and the drinking of 1,200 +/- 60 ml of water, over 85% of the mean cumulative water intake in the 30-min drinking period. Control studies in the same subjects showed comparable rises in plasma vasopressin, plasma osmolality, and thirst during hypertonic saline infusion but no fall in any of these parameters during an equivalent 30-min period after the infusions, during which water was withheld.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗