Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “THIRST”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources
PubMed1992

Abnormalities of thirst regulation in patients with chronic renal failure on hemodialysis.

To determine whether thirst mechanisms are altered in nondiabetic patients with chronic renal failure on hemodialysis, 4 patients with an average weight gain between dialysis sessions of more than 5% of dry body weight (group I), 5 patients with less than 3% weight gain (group II), and a group of 6 healthy subjects (group III) were submitted to infusion of hypertonic saline. After infusion the subjects had free access to water. Thirst was evaluated by visual analogue rating scales. Despite similar increments of effective plasma osmolality during saline infusion, patients of group I were thirstier than groups II and III (p less than 0.005 and p less than 0.01, respectively). Changes in thirst ratings were similar in groups II and III. Osmotic thresholds for thirst onset were similar in groups II and III (288.9 +/- 8.5 and 289.8 +/- 3.4 mosm/kg, respectively), but lower in group I (277.6 +/- 7.6 mosm/kg). Nevertheless, great variations were observed in the latter group. Thus, 2 patients showed thresholds for thirst within the normal range, whereas the others had low osmolar thresholds for thirst and baseline plasma osmolalities and high basal thirst scores. During the drinking period, the patients of group I drank more (14.2 +/- 2.8 ml/kg) than those of groups II (5.3 +/- 1.6 ml/kg; p less than 0.02) and III (10.2 +/- 1.6 ml/kg; n.s.) The plasma levels of angiotensin II in uremic patients were higher than in healthy subjects, although there were no differences between groups I and II and no correlation between basal angiotensin II levels and the interdialytic weight gain.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed2004

Thirst sensations and AVP responses at rest and during exercise-cold exposure.

PURPOSE: The purpose of this study was to 1) determine the effect of hypohydration (HYPO) on thirst sensations during moderate exercise in the cold and 2) determine a possible mechanism for a cold-induced decline in thirst. METHODS: In the first phase of the study, eight males walked on four occasions, in T-shirts, shorts, and shoes, at 50% VO2max, for 60 min in either a 4 degrees C (cold) or 27 degrees C (temperate) environment in a state of HYPO or euhydration (EU). In the second phase, nine males in states of EU or HYPO randomly performed four trials consisting of 30 min standing at 27 degrees C, followed by 30 min of standing and 30 min of treadmill exercise at 50% of VO2max, in either 4 degrees C or 27 degrees C air. RESULTS: In phase 1, thirst sensations were lower throughout 60 min of exercise (P < 0.05) in both HYPO and EU conditions during the cold trials. In phase 2, despite elevated plasma osmolality (P < 0.05), perception of thirst and plasma arginine vasopressin [AVP] similarly decreased (P < 0.05) after 30-min standing rest and 30-min exercise in the HYPO-cold trial, compared with the HYPO-temperate, EU-cold, and EU-temperate trials. CONCLUSIONS: When either euhydrated or hypohydrated, cold exposure attenuated thirst by up to 40% at rest and during moderate-intensity exercise. The attenuated thirst when hypohydrated during cold exposure was associated with lower plasma [AVP] despite an elevated plasma osmolality. This decline in thirst and AVP in the cold may be the result of peripheral vasoconstriction, mediating an increase in central blood volume and stimulation of central volume receptors.

Arginine Vasopressin↗
PubMed1998

Osmoregulation in clinical disorders of thirst appreciation.

Thirst and drinking are essential components of normal osmoregulation in healthy man. Abnormalities of thirst appreciation, in particular hypodipsia, have profound implications for water homeostasis. The combination of cranial diabetes insipidus and hypodipsia can have particularly serious consequences, with the potential for life-threatening hyponatraemia. Although the tools for measuring thirst are subjective and lack true specificity, their use in clinical research has contributed greatly to our understanding of the physiology of thirst appreciation and the abnormal control of thirst in osmoregulatory disorders. The precise neural control of thirst appreciation remains unknown, and perhaps as a result of this, satisfactory therapies for the treatment of disorders of thirst have not yet been developed; behavioural modification and retraining of drinking habits remain the rather limited cornerstones of management.

Adult↗
PubMed1971

Hypothalamic alpha- and beta-adrenergic systems regulate both thirst and hunger in the rat.

Adrenergic and adrenolytic drugs were injected directly into the hypothalamus of the rat brain through permanently implanted cannulas and were found to have reliable effects on water consumption in water-satiated and water-deprived subjects. The beta-adrenergic agonist stimulated thirst, and the beta-adrenergic blocker suppressed thirst. Conversely, the alpha-adrenergic agonist suppressed thirst, and the alpha-adrenergic blocker enhanced thirst. These results demonstrate the existence of a hypothalamic beta-adrenergic "thirst" system which opposes a hypothalamic alpha-adrenergic "water-satiety" system. In view of our earlier results demonstrating the existence in the hypothalamus of an alpha-adrenergic "hunger" system which opposes a beta-adrenergic "food-satiety" system, we suggest that a reciprocal inhibitory relationship between these adrenergic hunger- and thirst-regulating systems provides a neurochemical explanation for the ability of organisms to maintain food and water consumption at a constant ratio. In the regulation of both hunger and thirst, the central cholinergic system mimics the hypothalamic beta-adrenergic system and opposes the hypothalamic alpha-adrenergic system.

Adrenergic alpha-Agonists↗
PubMed1998

Determinants of the thirst-quenching character of beer.

The purpose of this study was to find which sensory characteristics are significant determinants of the thirst-quenching character of beer. The sensory attributes and thirst-quenching characteristics ("thirst quenching", "refreshing", "drinkability") of 18 beers were evaluated by a panel of 12 judges. The only significant positive determinants of the "thirst-quenching" character of the beers in the design were carbonation and bubble density. Significant negative determinants were foam, overall aroma and flavor, color, viscosity, malty, hoppy, burnt, bitterness, acidic, metallic, astringency and aftertaste. The same correlations (both in terms of direction and significance level) were observed between descriptive attributes and the "refreshing" and "drinkability" factors. A principal component analysis (PCA) of the mean ratings indicated that variability among beers was mostly along a thirst-quenching dimension (72% of the variance). Procrustes analysis performed on the individual ratings showed that, for one of the judges, the interpretation of the thirst-quenching concept differed from that shown by PCA for the overall panel.

Adult↗
PubMed1987

Osmotic thirst suppression in dogs exposed to low ambient temperature.

Body temperature, urine output, osmotic and free water clearances, plasma osmolality, sodium and potassium concentrations, blood lactate level, osmotic thirst and central blood volume were measured in dogs exposed to cold (+1 to -8 degrees C) for 1-3 hours and compared to those obtained under control conditions at ambient temperatures (18-20 degrees C). In some additional experiments osmotic thirst threshold and arterial blood pressure during intravenous infusion of norepinephrine were also examined. Exposure to low ambient temperature caused an increase in the osmotic thirst threshold and rise in central blood volume. Transient increase in the urine output and free water clearance accompanied by a decrease in the urine osmolality were also observed. No changes were found in rectal temperature, plasma osmolality and plasma sodium concentration. Infusion of norepinephrine elevated the osmotic thirst threshold in a dose-dependent manner. It is concluded that the cold-induced suppression of osmotic thirst may result from the increased central blood volume. A possible involvement of the sympathetic nervous system in the thirst inhibition in low ambient temperature is also considered.

Animals↗
PubMed2006

Water intake and the neural correlates of the consciousness of thirst.

Thirst and resultant water drinking can arise in response to deficits in both the intracellular and extracellular fluid compartments. Inhibitory influences mediating the satiation of thirst also are necessary to prevent overhydration. The brain regions that underpin the generation or inhibition of thirst in these circumstances can be categorized as sensory, integrative, or cortical effector sites. The anterior cingulate cortex and insula are activated in thirsty human beings as shown by functional brain-imaging techniques. It is postulated that these sites may be cortical effector regions for thirst. A major sensory site for generating thirst is the lamina terminalis in the forebrain. Osmoreceptors within the organum vasculosum of the lamina terminalis and subfornical organ detect systemic hypertonicity. The subfornical organ mediates the dipsogenic actions of circulating angiotensin II and relaxin. Major integrative sites are the nucleus of the tractus solitarius, the lateral parabrachial nucleus, the midbrain raphé nuclei, the median preoptic nucleus, and the septum. Despite these advances, most of the neural pathways and neurochemical mechanisms subserving the genesis of thirst remain to be elucidated.

Animals↗
PubMed1991

Thirst and plasma levels of vasopressin, angiotensin II and atrial natriuretic peptide in patients with non-insulin-dependent diabetes mellitus.

To clarify a possible mechanism whereby the perception of thirst may be associated with diabetes mellitus, we measured plasma levels of vasopressin (AVP), angiotensin II (ANG II), atrial natriuretic peptide (ANP) and plasma renin activity (PRA) in non-insulin-dependent (NIDDM) diabetic patients with or without thirst. Thirteen male NIDDM patients complaining of thirst had a significantly high blood hematocrit, plasma urea nitrogen and creatinine concentrations and plasma osmolality, indicating a reduction in plasma volume. In addition, the patients had a significantly high mean plasma concentrations of AVP (3.20 +/- 1.27 pmol/l) ANG II (33.8 +/- 31.4 pmol/l) and PRA, but a low mean plasma ANP concentration (8.9 +/- 4.5 pmol/l). After treatment with diet and/or sulfonylurea, plasma levels of AVP, ANG II and PRA decreased with a concomitant increase in plasma volume and disappearance of thirst. In contrast, 13 NIDDM patients (9 females and 4 males) without thirst had normal plasma urea nitrogen and creatinine concentrations, and the hematocrit did not change significantly after treatment. Plasma AVP (0.95 +/- 0.34 pmol/l), ANG II (14.7 +/- 8.8 pmol/l) and ANP (10.7 +/- 4.9 pmol/l) concentrations, and PRA were normal in this group of patients. There was no significant difference between the two groups of patients, however, in fasting glucose concentration and HbA1c. We conclude from these results that a reduction in plasma volume may be the major factor responsible for the induction of thirst sensation and for increased AVP secretion in NIDDM patients. The mechanism underlying a reduction in plasma volume remains unclear.

Adult↗
PubMed1980

Disordered control of thirst in hypothalamic-pituitary sarcoidosis.

We evaluated water metabolism in 11 patients with hypothalamic-pituitary sarcoidosis. Seven patients had abnormal water metabolism: one had partial antidiuretic hormone (ADH) deficiency, one had severe ADH deficiency, one had severe ADH deficiency and deficient thirst, one had only deficient thirst, and three had excessive thirst. In four of the five with thirst disturbances, there was loss of congruence of osmotic thresholds for thirst and ADH release. Five of our patients presented with polyuria and polydipsia, but only two had true diabetes insipidus, whereas three had organic primary polydipsia with adequate endogenous ADH. That disordered thirst resulting in polydipsia was more common than true diabetes insipidus is at odds with previously held views on the prevalence of ADH deficiency in this condition.

Adolescent↗
PubMed2006

Unique, common, and interacting cortical correlates of thirst and pain.

This study used positron-emission tomography to establish the patterns of brain activity involved in the isolated and concurrent experiences of thirst and pain. Ten subjects were scanned while experiencing pain evoked with noxious pressure, while experiencing thirst after the infusion of hypertonic saline, and while experiencing pain when thirsty. After the onset of thirst, noxious pressure evoked more intense sensations of pain. Noxious pressure did not change subjective ratings of thirst. Thirst caused activation in the anterior cingulate (Brodmann area 32) and the insula. Enhanced pain responses were associated with increased activity in cortical regions that are known to correlate with pain intensity, and also with unique activity in the pregenual anterior cingulate and ventral orbitofrontal cortex. These findings suggest a role for limbic and prefrontal cortices in the modulation of pain during the experience of thirst.

Adult↗
PubMed1985

Osmotic thirst and vasopressin release in humans: a double-blind crossover study.

Thirst is a subjective sensation. Therefore to investigate further the nature, intensity, and specificity of osmotic thirst, we studied the effects of double-blind infusions of hypertonic (0.45 M) and isotonic (0.15 M) saline on subjective ratings and sensations of thirst, water intake, plasma vasopressin, and body fluids in seven healthy volunteer young men. Only the hypertonic saline significantly increased plasma sodium concentration, plasma osmolality, plasma vasopressin concentration, and visual analog ratings of thirst sensations. Both infusions expanded blood volume, which was greater with the hypertonic saline infusion. Neither solution significantly altered mean arterial blood pressure nor plasma angiotensin levels. Throughout a 60-min drinking period after the infusions, water intake was always significantly greater after the hypertonic saline than after the isotonic saline. The subjects described the thirst sensations as mainly due to a dry unpleasant tasting mouth, which was promptly relieved by drinking. Visual analog rating changes confirmed the subjective reports. Finally, the effects on thirst and vasopressin secretion were observed at plasma sodium concentration and osmolality changes that are well within the physiological range.

Adult↗
PubMed1991

Reduced osmotic thirst in healthy elderly men.

In response to water deprivation or heat stress, healthy elderly men experience reduced thirst compared with a young control group. Because water deprivation and heat stress produce hypertonicity as well as reduced extracellular fluid volume, the aim of this study was to determine whether the elderly also experience reduced thirst in response to hypertonicity without extracellular fluid volume depletion. To achieve this, after an overnight fast, healthy community-dwelling nonsmoking old (65-78 yr, n = 7) and young (20-32 yr, n = 7) men received 120-min hypertonic (0.855 M) and isotonic (0.154 M) saline infusions (0.06 ml.min-1.kg-1) in double-blind randomized order at least 2 wk apart. Both groups had increased thirst (P less than 0.001) and water intake (P less than 0.05) after the hypertonic saline infusion compared with the isotonic saline infusion. However, despite similar plasma sodium increases and less plasma volume expansion during the hypertonic saline infusion compared with the young group, the old group was less thirsty (P less than 0.01) and drank less room-temperature tap water (young 11.1 +/- 1.2 ml/kg, old 3.9 +/- 0.6 ml/kg, P less than 0.001). This reduced thirst in the old group seemed to be mainly due to a lower thirst sensitivity (P less than 0.05) to hypertonicity, although there was also a tendency toward an increased thirst threshold. Plasma arginine vasopressin increases were similar for the old and young groups with hypertonic saline, without significant changes during the isotonic saline infusion in either group.

Adult↗
PubMed1993

Effects of drinking on thirst and vasopressin in dehydrated elderly men.

Inhibition of dehydration-induced arginine vasopressin (AVP) secretion and thirst depends on removal of osmotic and hemodynamic stimuli as well as on preabsorptive oropharyngeal factors that reduce thirst and AVP secretion on drinking before correction of the water deficits. Plasma atrial natriuretic peptide (ANP) levels may also change with drinking. Therefore, the thirst and plasma responses to oral water loads (10 ml/kg) in 10 healthy old (64-76 yr) and young (20-32 yr) 24-h water-deprived men were investigated. After 24-h water deprivation plasma sodium, osmolality, and AVP were increased similarly in both groups (P < 0.001). Plasma ANP levels fell after dehydration similarly in both groups (P < 0.05) but were always higher in the older group (P < 0.05). However, although thirst increased in both groups (P < 0.05), this was significantly less in the elderly (P < 0.05). After the water load, thirst was reduced in both groups throughout the study (P < 0.05). However, plasma AVP fell immediately after drinking only in the young group and rose to postdeprivation levels after 15 min. Plasma AVP was not different from postdeprivation throughout in the old group and after 15 min in the young group presumably because the water load was insufficient to replace their water deficits. In the young group only, plasma ANP rose to 182 +/- 43% of postdeprivation levels at 3 min after drinking (P < 0.05). These results demonstrate reduced oropharyngeal inhibition of AVP secretion after drinking in healthy elderly men but maintained inhibition of thirst.

Adult↗
PubMed1994

Body fluid balance in dehydrated healthy older men: thirst and renal osmoregulation.

We examined osmotic control of thirst and free water clearance in healthy older (65+, n = 10) and younger (Y, n = 6) subjects during a 3-h rehydration period after an approximately 2.4% decrease in body weight. Plasma volume (PV), plasma osmolality (Posm), renal function, and thirst were measured before and after dehydration and during rehydration. In 65+, baseline PV was lower (43.1 +/- 1.6 vs. 48.1 +/- 2.5 ml/kg), Posm was higher (287 +/- 1 vs. 281 +/- 2 mosmol/kgH2O), and perceived thirst was lower than in Y. During dehydration, the osmotic threshold for increased thirst was shifted to a higher Posm in 65+. Total fluid intake was greater in Y than in 65+ (16.6 +/- 4.1 vs. 8.9 +/- 2.0 ml/kg); however, the relation between thirst and the rate of fluid intake was identical. Thus the blunted rehydration in 65+ is related to a lower overall sensation of thirst. The stimulus-response characteristics of osmotic control of free water clearance was similar in 65+ and Y; however, 65+ operated around a higher Posm and on a less-steep portion of the stimulus-response curve. These data support the hypothesis that the hyperosmotic hypovolemic state of healthy older individuals is not a result of a simple water deficit but represents a shift in the operating point for control of body fluid volume and composition.

Adolescent↗
PubMed1981

Enhancement of osmotic thirst elicited by electric stimulation of the limbic system in dogs.

Seven dogs were chronically implanted with 30 electrodes directed at various structures of the basal forebrain. Osmotic thirst threshold (expressed as an increase in plasma osmolality and a decrease in cellular water content caused by an intravenous infusion of 5% NaCl, necessary to induce drinking) was measured during electric stimulation of the basal forebrain and compared to that found under control conditions. Stimulation through 11 electrodes located in the lateral part of the septum (5 locations) and other parts of the limbic system markedly decreased the osmotic thirst threshold. The increment in plasma osmolality necessary to elicit drinking decreased from 9.7 +/- 1.3 to 4.8 +/- 1.2 mmol/kg (n = 11). The volume of water drunk at the thirst threshold did not differ significantly. A significant augmentation of the volume of water drunk during 1 h following infusion of hypertonic saline was observed when the infusion was combined with stimulation of the gyrus rectus, precommissural septum and nucleus accumbens. These and previous results (SZCZEPANSKA-SADOWSKA et al., 1979) suggest that the limbic system of the basal forebrain exerts both excitatory and inhibitory influences on the thirst system. The prolonged poststimulatory overdrinking indicates that enhancement of osmotic thirst cannot be entirely explained by an immediate action of the stimulating current on the neurons of the thirst system.

Animals↗
PubMed1995

The sensation of thirst in dying patients receiving i.v. hydration.

Cancer patients in the terminal phase of their disease often experience fluid deficits. This is mainly due to their inability to ingest adequate amounts of oral fluids to meet the body's physiological demands. In order to correct this deficit, intravenous (i.v.) fluid programs are often instituted. This pilot study was conducted on a group of terminal patients hospitalized in an oncology unit who died while receiving i.v. fluids. It sought to assess the effects of these fluids on their level of thirst. Data were collected on 30 patients in the last 24 hours of life. However, of the 30 patients only 19 were sufficiently alert to be able to verbally evaluate their thirst intensity. Of the 19 patients, six experienced mild thirst, eight moderate thirst, and four severe thirst. This was in spite of IAV hydration regimens which ranged from 500 mL to 3000 mL. Little relationships was found between level of thirst and the amount of i.v. fluids received, blood urea nitrogen (BUN), or sodium blood levels. In addition, although 70% of the patients had fluid retention signs, there was little correlation between these signs and the amount of fluids received. Since the pilot study's sample was small, definitive conclusions could not be drawn. However, our results highlight the need for future research in this area.

Adult↗
PubMedDate not supplied

Pharmacotherapy in congestive heart failure: angiotensin II and thirst: therapeutic considerations.

Angiotensin II is the effector peptide of the renin-angiotensin system and is involved in a wide range of physiologic functions that relate to volume control. In this regard, angiotensin II maintains and regulates salt and water balance, is critically involved in cardiovascular function, and governs thirst. When present in excess, angiotensin II can pathologically influence each of these functions. The role of angiotensin II in controlling sodium balance, in both renal insufficiency states and congestive heart failure, is clearly recognized. Alternatively, it is poorly appreciated that angiotensin II plays an important role in both normal and pathologic thirst states. The latter is a potential problem in both end-stage renal disease and congestive heart failure. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor antagonists (AT1-RAs) have both been shown to reduce abnormal thirst drive. Whether an ACE inhibitor or an AT1-RA lessens thirst drive to any significant degree relates to its capacity to penetrate the blood-brain barrier. Head-to-head comparisons of ACE inhibitors and AT1-RAs, as to their effect on thirst drive, have not been undertaken in a systematic fashion; thus, until otherwise established, the effect of these compounds on thirst should be viewed as a class effect, albeit one that is likely to be dose-dependent. (c)2001 CHF, Inc.

Journal Article↗
PubMed1985

Interaction between cholinergic and adrenergic synapses of the rat subfornical organ and the thirst-inducing effect of angiotensin II.

Previous studies by our group and other authors have demonstrated that application of carbachol or angiotensin II to the subfornical organ (SFO) of satiated rats causes an intense thirst-inducing response. It has also been demonstrated that muscarinic cholinergic synapses are mainly involved in the thirst-inducing effect of carbachol, with a secondary role played by nicotinic receptors. The beta-adrenergic pathways of the SFO have also been shown to participate in the regulation of water intake. The present study was designed to investigate the possible interaction between cholinergic and adrenergic neurons of the subfornical organ and the effect of angiotensin II and carbachol in the regulation of water intake by this structure. The intense water intake induced by injection of 2 nmol carbachol into the SFO was markedly reduced when different doses of propranolol (20, 40, 80, and 160 nmol) were previously injected. The response to carbachol, however, was not changed by previous treatment with regitine (20, 40, and 80 nmol). Injection of 0.1 to 4.0 ng angiotensin II into the SFO caused a dose-dependent increase in water intake. When the 4 ng dose of angiotensin was injected into the SFO after an injection of atropine (20, 40, and 80 nmol), complete absence of water intake was observed, the same occurring when propranolol was previously injected at doses of 40 and 80 nmol. The thirst-inducing effect of angiotensin II (4 ng) was not changed by previous injection of hexamethonium (20, 40, 80, and 160 nmol) or phentolamine (20, 40, and 80 nmol). These results permit us to suggest that angiotensin II and carbachol induce thirst when applied to the SFO by acting through independent systems. The participation of beta-adrenergic receptors in the thirst-inducing effect of angiotensin II and carbachol was also demonstrated, as well as the participation of muscarinic cholinergic receptors in the thirst-inducing effect of angiotensin II injected into the SFO.

Angiotensin II↗