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 91 records · Page 5Linked to original sources
PubMed1998

Angiotensin, thirst, and sodium appetite.

Angiotensin (ANG) II is a powerful and phylogenetically widespread stimulus to thirst and sodium appetite. When it is injected directly into sensitive areas of the brain, it causes an immediate increase in water intake followed by a slower increase in NaCl intake. Drinking is vigorous, highly motivated, and rapidly completed. The amounts of water taken within 15 min or so of injection can exceed what the animal would spontaneously drink in the course of its normal activities over 24 h. The increase in NaCl intake is slower in onset, more persistent, and affected by experience. Increases in circulating ANG II have similar effects on drinking, although these may be partly obscured by accompanying rises in blood pressure. The circumventricular organs, median preoptic nucleus, and tissue surrounding the anteroventral third ventricle in the lamina terminalis (AV3V region) provide the neuroanatomic focus for thirst, sodium appetite, and cardiovascular control, making extensive connections with the hypothalamus, limbic system, and brain stem. The AV3V region is well provided with angiotensinergic nerve endings and angiotensin AT1 receptors, the receptor type responsible for acute responses to ANG II, and it responds vigorously to the dipsogenic action of ANG II. The nucleus tractus solitarius and other structures in the brain stem form part of a negative-feedback system for blood volume control, responding to baroreceptor and volume receptor information from the circulation and sending ascending noradrenergic and other projections to the AV3V region. The subfornical organ, organum vasculosum of the lamina terminalis and area postrema contain ANG II-sensitive receptors that allow circulating ANG II to interact with central nervous structures involved in hypovolemic thirst and sodium appetite and blood pressure control. Angiotensin peptides generated inside the blood-brain barrier may act as conventional neurotransmitters or, in view of the many instances of anatomic separation between sites of production and receptors, they may act as paracrine agents at a distance from their point of release. An attractive speculation is that some are responsible for long-term changes in neuronal organization, especially of sodium appetite. Anatomic mismatches between sites of production and receptors are less evident in limbic and brain stem structures responsible for body fluid homeostasis and blood pressure control. Limbic structures are rich in other neuroactive peptides, some of which have powerful effects on drinking, and they and many of the classical nonpeptide neurotransmitters may interact with ANG II to augment or inhibit drinking behavior. Because ANG II immunoreactivity and binding are so widely distributed in the central nervous system, brain ANG II is unlikely to have a role as circumscribed as that of circulating ANG II. Angiotensin peptides generated from brain precursors may also be involved in functions that have little immediate effect on body fluid homeostasis and blood pressure control, such as cell differentiation, regeneration and remodeling, or learning and memory. Analysis of the mechanisms of increased drinking caused by drugs and experimental procedures that activate the renal renin-angiotensin system, and clinical conditions in which renal renin secretion is increased, have provided evidence that endogenously released renal renin can generate enough circulating ANG II to stimulate drinking. But it is also certain that other mechanisms of thirst and sodium appetite still operate when the effects of circulating ANG II are blocked or absent, although it is not known whether this is also true for angiotensin peptides formed in the brain. Whether ANG II should be regarded primarily as a hormone released in hypovolemia helping to defend the blood volume, a neurotransmitter or paracrine agent with a privileged role in the neural pathways for thirst and sodium appetite of all kinds, a neural organizer especially in sodium appetit

Angiotensin II↗
PubMed1981

Increased thirst and plasma arginine vasopressin levels during 2-deoxy-D-glucose-induced glucoprivation in humans.

Insulin-induced hypoglycemia by unknown mechanism(s) increases plasma arginine vasopressin (AVP) levels in humans. Mechanisms for increased AVP levels during central nervous system glucoprivation were investigated by administering 20-min i.v. infusions of 2-deoxy-d-glucose (50 mg/kg), a competitive inhibitor of glucose utilization, or normal saline (sham), to 24 normal volunteers. Some of the infusions were administered in combination with neuropharmacological blocking agents (placebo). The behavioral, physiological, metabolic, and hormonal correlates of 2-deoxy-d-glucose (2DG)-induced gluco-privation and AVP secretion were studied in a group (n = 5) pretreated for 1 wk with either mazindol (1 mg per os three times per day), a potent norepinephrine and dopamine-reuptake blocker, or placebo. A second group (n = 5) received either propranolol (3 mg/3 min followed by 80 mug/min) or normal saline infusion before and during 2DG administration. With 2DG alone, plasma AVP levels increased from 1.3+/-0.3 pg/ml at base line to a peak of 4.5+/-1.4 pg/ml at 60 min and remained elevated for 150 min. From 30 to 180 min after 2DG administration, the 2DG-infused volunteers increased their water intake in comparison with sham-infused volunteers. Marked increases in epinephrine and slight increases in norepinephrine were associated with increases in plasma glucose and renin activity and decreases in plasma potassium. Plasma sodium and osmolality increased transiently and mean arterial pressure (MAP) fell. These changes, however, were small and inconstant and could not account for the observed increases in thirst and AVP levels. Pretreatment with mazindol prevented the decrease in MAP and the increase in plasma renin activity (PRA) following 2DG infusions without modifying increased thirst, water intake, or AVP responses to glucoprivation. Pretreatment with propranolol effectively blocked beta-adrenoreceptors as evidenced by increased MAP and plasma epinephrine, and abolition of the RPA increases during 2DG-induced glycoprivation, but did not suppress AVP and thirst responses. A cervical cord-sectioned patient lacking descending sympathetic out-flow had a potentiated thirst response to 2DG-induced glucoprivation in the absence of increases in sodium, catecholamines, and PRA. Thus 2DG administration activates mechanisms for increased thirst and AVP which are unrelated to changes in peripheral catecholamines, MAP, PRA, and osmolality.

Arginine Vasopressin↗
PubMed1988

Serial evaluation of vasopressin release and thirst in human pregnancy. Role of human chorionic gonadotrophin in the osmoregulatory changes of gestation.

Serial studies were designed to characterized changes in osmoregulation throughout gestation. Eight women underwent a 2-h infusion of hypertonic saline before conception, during gestational weeks 5-8, 10-12, and 28-33, and then 10-12 wk postpartum. Basal plasma osmolality (Posmol) was already significantly decreased by 5-8 wk (P less than 0.001) and remained 10 mosmol.kg-1 below nonpregnant values throughout pregnancy. The apparent threshold for AVP release (defined as the abscissal intercept of the regression line relating plasma AVP [PAVP] to Posmol) was also decreased significantly throughout gestation, as was the osmotic threshold for thirst (derived from analogue scales relating desire to drink to Posmol). The decrement in osmotic thirst threshold appeared to precede that for AVP release, and consistent with this 24-h urine volumes were significantly greater at 5-8 wk gestation (P less than 0.05). The slopes of each regression equation defining PAVP vs. Posmol (whose r values ranged from 0.79 to 0.99), very reproducible before and after pregnancy, were similar at 5-8 and 10-12 wk, but were markedly reduced in the third trimester (P less than 0.001). These volunteers had randomly undergone an additional infusion before conception (both tests in the luteal phase of the menstrual cycle) when 10,000 IU of human chorionic gonadotrophin (hCG) had been given intramuscularly over a 5-d period. Serum hCG values between 0.2 and 3.3 U.ml-1 were lower than usually seen in pregnancy, but the osmotic thresholds for AVP release and thirst decreased by 3 and 4 mosmol.kg-1, respectively (P less than 0.05). Finally we studied a patient with a molar pregnancy in whom thresholds for hormone release and thirst were both decreased to values resembling normal gestation and remained so for approximately 6 wk postevacuation, only normalizing when hCG had virtually disappeared from her serum. In contrast, thresholds increased within the first two puerperal weeks in two women with normal pregnancies. These data demonstrate (a) osmotic thresholds for both AVP release and thirst decrease within the very first gestational weeks; (b) increment in PAVP per unit increase in Posmol is reduced late in gestation; and (c) hCG may be involved in the osmoregulatory changes of pregnancy.

Adolescent↗
PubMed2002

Development of the thirst distress scale.

This article describes the development of a 6-item instrument that measures thirst distress. Items were developed following open-ended interviews with 10 subjects, a literature review, and development of a conceptual definition of thirst. A panel of experts established content validity. A convenience sample (N = 247) of adults receiving outpatient hemodialysis completed the scale. A panel of experts was used to assess content validity. Item analysis was used to select unrelated or redundant items for deletion. Cronbach's alpha was .78. Construct validity was supported by confirmatory and exploratory factor analysis. Positive relationships between thirst distress and, respectively, thirst intensity and interdialytic weight gain provided additional evidence of construct validity. Overall, these preliminary data indicate that the thirst distress scale has sufficient reliability and validity for use in clinical studies.

Adult↗
PubMed1998

[Acquired disorder of thirst perception with intact osmoregulation of vasopressin].

We report a 45 y old male patient with severe hypodipsia, but intact vasopressin secretion and maximal renal response to vasopressin. The patient presented during hot summer days, 18 months after a frontal lobe hemorrhage due to a ruptured aneurysm, with severe hypernatremia (171 mmol/L) and a plasma osmolality of 348 mosm/kg. He was awake and had no interest in fluid intake. After initial correction, a thirst test for 36 hours was performed. Plasma osmolality rose from 295 to 320, urine osmolality rose from 220 to 700 mosm/kg, while plasma vasopressin levels increased more than 3-fold. Throughout the test the patient did not exhibit appreciable thirst. The intact osmoregulation of vasopressin as evidenced by the plasma levels and the elicited renal response, indicates that a selective acquired disturbance of thirst is present. Whether the thirst center is destroyed or/and thirst recognition (frontal lobe affection) is disturbed primarily, can not be decided.

Aneurysm, Ruptured↗
PubMed1994

Intracerebroventricular injection of renin in the neonatal rat reveals a precocious sodium appetite that is dissociated from renin-aroused thirst.

Previous research on the ontogeny of sodium appetite in the rat has shown that sodium deficit first engenders sodium intake at 12 days of age, whereas direct stimulation of the brain renin--angiotensin system by intracranial injection of renin increases intake of NaCl solution as early as 3 days postnatally. Similar activation of brain angiotensin also increases thirst, so that the specificity of the precocious sodium intake remains undetermined. In this article we report experiments that dissociate neonatal renin-evoked sodium appetite and thirst, and establish the specificity of the appetite. Our findings confirm that sodium appetite can first be discerned at 3 days of age, and show that it rapidly develops until 12 days of age. During this developmental window, renin-evoked sodium appetite is dissociated from thirst because (a) NaCl is preferred to water, (b) the appetite develops faster than thirst, and (c) 3-day-old renin-stimulated pups will avidly lick dry NaCl. These results show that activation of brain angiotensin in the 3-day-old rat pup evokes a precocious and specific sodium appetite.

Age Factors↗
PubMed1997

Effects of temperature and volume on measures of mouth dryness, thirst and stomach fullness in males and females.

The immediate post-ingestive effects of temperature on thirst reduction were explored. Thirst was assessed by both ratings and a volume selection task. Supplementary ratings assessed mouth dryness and stomach fullness. All measures were taken before and 0, 2.5 and 5 min after drinking one of four water samples (150 ml/5 degrees C, 400 ml/5 degrees C, 150 ml/22 degrees C or 400 ml/22 degrees C). After 2.5 min, the cold sample produced greater reductions than the warmer sample in (i) the thirst ratings of males who received 400-ml samples, and (ii) the volume selections of females who received 150-ml samples. It is proposed that temperature influenced thirst reduction because of its differential effects on the post-ingestive state of the mouth.

Adult↗
PubMed2000

The awareness of thirst: proposed neural correlates.

The neural and endocrine bases of the generation of thirst are reviewed. Based on this review, a hierarchical system of neural structures that regulate water conservation and acquisition is proposed. The system includes primary sensory-receptive areas; secondary sensory structures (circumventricular organs), which detect levels of hormones, including angiotensin II and vasopressin, which are involved in generating thirst; preoptic and hypothalamic structures; and an area within the ventrolateral quadrant of the periaqueductal gray matter. Hodological and other data are used to determine the hierarchical organization of the system. Based on studies of the effects of lesions to various structures within the hierarchy of the system, it is proposed that the awareness of thirst in rodents is either entirely or predominantly due to neuronal activities in a subsection of the ventrolateral periaqueductal gray matter. It is also hypothesized that the awareness of thirst in primates is due to neuronal activities in both the ventrolateral periaqueductal gray and in a region within the medial prefrontal and anterior cingulate cortex.

Angiotensin II↗
PubMed1999

Exaggerated vasopressin secretion and attenuated osmoregulated thirst in human survivors of hyperosmolar coma.

AIMS/HYPOTHESIS: To test the hypothesis that subnormal thirst sensation could contribute to the development of the hypernatraemia characteristic of hyperosmolar coma, we studied osmoregulation in survivors of hyperosmolar coma. METHODS: Eight survivors of hyperosmolar coma, eight control subjects with Type II (non-insulin-dependent) diabetes mellitus and eight healthy control subjects underwent water deprivation during which measurements of thirst, plasma osmolality and vasopressin were taken. RESULTS: Water deprivation caused greater peak plasma osmolality in the hyperosmolar coma group (301.7 +/- 2.7 mmol/kg) than in Type II diabetic (294.3 +/- 3.2 mmol/kg, p < 0.01) or control group (296.9 +/- 3.0 mmol/kg, p < 0.01) and a greater increase in plasma vasopressin concentration (hyperosmolar coma, 5.8 +/- 1.3 pmol/l, Type II diabetes, 1.8 +/- 1.3 pmol/l, p < 0.001, control subjects, 2.2 +/- 1.8 pmol/l, p < 0.001). Thirst ratings were lower following water deprivation in the hyperosmolar coma group (3.5 +/- 0.8 cm) than in Type II diabetes (7.7 +/- 1.6 cm, p < 0.001) or control subjects (7.4 +/- 1.3 cm, p <0.001), and the hyperosmolar group patients drank less in 30 min following water deprivation (401 +/- 105 ml) than Type II diabetic (856 +/- 218 ml, p < 0.001) or control subjects (789 +/- 213 ml, p < 0.001). CONCLUSION/INTERPRETATION: Survivors of hyperosmolar coma have subnormal osmoregulated thirst and fluid intake, which might contribute to the hypernatraemic dehydration typical of the condition.

Aged↗
PubMed1984

Body fluid changes, thirst and drinking in man during free access to water.

To investigate whether human thirst and drinking during ad lib access to water occur in response to body fluid deficits, we obtained blood samples and visual analog scale thirst ratings from five healthy, volunteer, young men at hourly intervals and when they were thirsty during a normal working day. Although there were significant increases in ratings of thirst, pleasantness of drinking water, mouth dryness and unpleasantness of the taste in the mouth when subjects were thirsty enough to drink compared with intervening intervals, there were no concomitant changes in body fluid variables (microhematocrit, plasma osmolality and plasma sodium, potassium, protein and angiotensin II concentrations). Subjects drank mainly in association with eating and were not overhydrated as indicated by constantly hypertonic urine and significant tubular reabsorption of free water over the experimental period. The results indicate that during free access to water humans become thirsty and drink before body fluid deficits develop, perhaps in response to subtle oropharyngeal cues, and so provide evidence for anticipatory thirst and drinking in man.

Adult↗
PubMed1995

Intracerebroventricular administration of angiotensin type 1 (AT1) receptor antisense oligonucleotides attenuate thirst in the rat.

The central actions of the peptide hormone angiotensin II (AngII) are importantly involved in body fluid homeostasis. Included amongst these actions is a potent dipsogenic response that has been implicated in the thirst that develops during many forms of extracellular dehydration. The use of highly selective receptor antagonists has revealed that the Type 1 (AT1), and not the Type 2 (AT2), AngII receptor subtype mediates this drinking response. More recently, antisense oligonucleotides specific for the AT1 receptor have been developed and after intracerebroventricular (i.c.v.) administration, they significantly reduce the dipsogenic response elicited by a similar injection of AngII. In the present study AT1 antisense oligonucleotides were used to further investigate their effect on experimentally induced thirst in the rat. In addition, immunohistochemical analysis of biotin-labeled oligonucleotides was performed in order to correlate the behavioral effects of the oligonucleotides with their distribution in the brain. The results demonstrated that the antidipsogenic effects of the oligonucleotides were dose and time-dependent and were limited to those thirst challenges that involve activation of the renin-angiotensin system. Collectively, these results demonstrate the efficacy and behavioral specificity of these oligonucleotides, as well as their utility in investigating the physiological role of cerebral AngII receptor subpopulations in various models of thirst.

Analysis of Variance↗
PubMedDate not supplied

Thirst impairment elicited by intraventricular administration of vasopressin antagonists.

To determine whether centrally released vasopressin influences thirst, observations of osmotic thirst threshold, osmotic load excretion and postloading restitution of plasma osmolality were made in dogs in control experiments and during infusion of AVP antagonists into the third ventricle. Significant elevation of osmotic thirst threshold was elicited by infusion of d(CH2)5AVP at a rate of 0.2-2.0 micrograms.min-1 and of d(Et2)AVP at a rate of 0.3 micrograms.min-1 (V1 antagonists, weak V2 agonists) as well as by administration of d(CH2)5[D-Ile2,Abu4]AVP at a rate of 0.4 micrograms.min-1 (potent V2 antagonist, weak V1 antagonist). Administration of d(CH2)5AVP at a rate of 2.0 micrograms.min-1 was associated with a significant suppression of the postloading water intake and osmotic load excretion and with a delay in restitution of plasma osmolality. These findings indicate that centrally released vasopressin may participate in the control of thirst.

Animals↗
PubMed2003

Hunger, thirst, and energy intakes following consumption of caloric beverages.

Whereas soft drinks are described as primarily thirst-quenching liquids, juices and milk are said to be liquid foods, with a greater satiating power. This study was conducted to compare the effects of orange juice, low-fat milk (1%), regular cola, and sparkling water on hunger, thirst, satiety, and energy intakes at the next meal. Thirty-two volunteers (14 men and 18 women), ages 18-35 years, consumed a breakfast preload composed of 590 ml (20 oz) of an energy-containing beverage (1036 kJ) or water (0 kJ) and a slice of toast (418 kJ) on four different occasions. Participants rated hunger, thirst, fullness, and desire to eat at baseline and at 20-min intervals for 2 h following preload ingestion. A tray lunch was presented at 2 h, 15 min and food consumption was measured. Compared to sparkling water, the three energy-containing beverages were associated with higher fullness and reduced hunger rating and desire to eat. However, energy intakes at lunch (4511+/-151 kJ for men and 3183+/-203 kJ for women) were the same across all four beverage conditions and no compensation for breakfast energy was observed. The three beverages of equal energy value were significantly different from sparkling water, but not from each other, in their effects on hunger and satiety ratings. All four beverages satisfied thirst equally well. Whether energy-containing cola, juice, and low-fat milk facilitate a positive energy balance remains a topic for further study.

Adult↗
PubMed2001

Drinking related direct current positive potential shift in the human EEG depends on thirst.

Scalp recorded direct current (DC)-potential shifts were examined in 11 human subjects who had either thirsted for 16 h or had quenched thirst before recordings. The recording epoch included a 3-min baseline, an interval of about 5 min during which subjects drank 400 ml of water, and a 7-min post-drinking interval. Consistent with previous data, when thirsty, subjects displayed a widespread negative DC-potential shift during drinking which was replaced by a positive DC shift at the transition to the post-drinking interval. The positivity after drinking lasted for about 2 min and averaged 146 microV at frontal recording sites. Quenching thirst before recordings reduced the positive DC-potential shift upon drinking, whereas changes in preceding drinking related DC negativity appeared to be secondary. The post-drinking positive DC-potential shift depending on the subject's motivational state can be considered an indicator of reward associated with quenching thirst, pointing to a lowered frontocortical excitability during reward.

Adult↗
PubMed1984

Thirst and sodium appetite after colloid treatment in rats with septal lesions.

Previous experiments in which angiotensin II (AII) and mineralocorticoids were administered to rats have suggested that these hormones play a natural role in mediating thirst and sodium appetite. This hypothesis was examined by making use of rats with septal lesions, which have an apparent sensitivity to the central effects of AII, and studying their behavioral response to subcutaneous colloid treatment, which produces hypovolemia and thereby stimulates the secretions of renin and aldosterone. The induced thirst and sodium appetite both were markedly enhanced in the brain-damaged animals. However, water intake was not increased when the hypovolemia was moderate, and sodium appetite was augmented only when animals had been sodium deprived, a procedure known to potentiate aldosterone secretion. These findings support previous suggestions that whereas AII normally contributes little to thirst, it may help to mediate sodium appetite in rats when aldosterone is abundant. Finally, the two drives were not elicited uniformly; those animals that drank the most water after colloid treatment consumed the least saline. These findings suggest that whereas septal lesions may sensitize the rat's brain to the sodium-appetite-eliciting effects of AII as well as to its dipsogenic effects, sodium appetite emerges only if the induced thirst is not too pronounced.

Aldosterone↗
PubMed1985

Angiotensin II-induced thirst and vasopressin release in man.

1. The thirst and plasma vasopressin responses to single-blind controlled intravenous angiotensin II infusions (2-16 ng min-1 kg-1) were investigated in ten healthy young men. 2. Thirst and vasopressin secretion were stimulated in four out of ten subjects. These effects occurred at plasma angiotensin concentrations well above those measured under physiological conditions associated with thirst and vasopressin secretion such as water deprivation. 3. Further studies are needed to define why only certain individuals respond to intravenous angiotensin II infusions and to determine whether potentiation of angiotensin-induced thirst and vasopressin secretion by other stimuli (e.g. hypovolaemia and hypertonicity) might occur in man, in particular under pathological conditions when plasma angiotensin levels are above the physiological range.

Adult↗
PubMed2006

Candesartan cilexetil on regular hemodialysis: inability to reduce excessive thirst, but good tolerance and efficacy in hypertensive patients.

It has been postulated that hypertension and interdialytic weight gain in hemodialysis patients are related to the activation of the renin-angiotensin system. Angiotensin II type 1 (ATI) receptor antagonists are new anti-hypertensive agents and are currently the most specific means of blocking the renin-angiotensin enzymatic cascade. Recent studies show that candesartan cilexetil regulates thirst and hypertension in rodents, via cerebral AT1 receptor blockade. We therefore conducted a prospective open study of candesartan cilexetil in 21 hypertensive patients on long-term hemodialysis during 6 weeks, focusing on thirst regulation. We also performed a prospective follow-up study of tolerance of candesartan and its anti-hypertensive efficacy after this 6-week study, while the patients remained on this therapy. Weight gain between hemodialysis sessions did not differ between the periods before and during candesartan cilexetil therapy. Median absolute interdialytic weight gain was 2.35 kg (range: 0.55-5) before therapy, compared to 2.25 kg (range: 0.35-4.65) during therapy (p > 0.05, Wilcoxon test). The median interdialytic weight gain/dry weight index was 3.7% (range: 1.15-7) before therapy and 3.6% (range: 0.7-6.6) during candesartan therapy (p > 0.05, Wilcoxon test). The median dose of candesartan cilexetil was 12 mg/day (range: 4-24). The median total duration of therapy with candesartan (including the 6 weeks of the thirst study) was 12 months (range: 2-25). During candesartan cilexetil therapy, the number of concomitant anti-hypertensive drugs per patient fell significantly (median number of anti-hypertensive drugs before candesartan =2 (range: 1-6); during candesartan =1 (range: 1-5) (p < 0.02, Wilcoxon test). No anaphylactoid reactions occurred. A total of 161 episodes of hypotension (5%) occurred during 3074 hemodialysis sessions (including the 6 weeks of the thirst study) We conclude that, like angiotensin converting enzyme inhibitors and the other angiotensin receptor antagonists, candesartan cilexetil is unable to reduce interdialytic weight gain in hemodialysis patients. This study also shows that the irreversible angiotensin II receptor antagonist candesartan cilexetil is a safe and effective therapeutic option for hypertensive hemodialysis patients.

Adult↗
PubMed2002

Lack of effect of long-term use of angiotensin-converting enzyme inhibitors by hemodialysis patients on thirst and fluid weight gain.

Volume overload is a chronic, troublesome problem in many patients on hemodialysis. These patients suffer from hyperdipsia with inability to excrete water. Angiotensin-converting enzyme inhibitor (ACEI) has been shown to decrease thirst and interdialytic weight gain in 2-4 weeks of usage. We investigated the effect of long-term use of ACEI, as levels of angiotensin II tends to go back to normal level after 6 months of use. We compared hemodialysis patients on ACEI for more than 6 months to patients not on ACEI. Seven patients were taking ACEI compared to 51 controls in the other group. Almost one third of patients in each group had an interdialytic weight gain > 5% of dry weight. No significant difference was found between the two groups with regard to interdialytic weight gain, thirst and mouth dryness scores, and interdialytic mean blood pressure change. There was no demonstrable effect of angiotensin receptor blocking drugs on weight gain or thirst. We conclude that long-term ACEI may not continue to suppress inappropriate thirst and fluid intake after 6 months in hemodialysis patients.

Angiotensin-Converting Enzyme Inhibitors↗