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At least 199 records · Page 11Linked to original sources
PubMed2002

Fos-like immunoreactivity and thirst following hyperosmotic loading in rats with subdiaphragmatic vagotomy.

If receptors in the gut relay information about increases in local osmolality to the brain via the vagus nerve, then vagotomy should diminish this signaling and reduce both thirst and brain Fos-like immunoreactivity (Fos-ir). Water intake in response to hypertonic saline (i.p. or i.g., 1 M NaCl, 1% BW; i.g., 0.6 M NaCl, 0.5% BW) was reduced during 120 min in rats with subdiaphragmatic vagotomy (VGX) compared to sham-VGX rats. Brain Fos-ir was examined in response to both i.g. loads. After the smaller load, VGX greatly reduced Fos-ir in the supraoptic nucleus (SON) and the magnocellular and parvocellular areas of the paraventricular nucleus (PVN). Fos-ir in the subfornical organ (SFO) and nucleus of the solitary tract (NTS) was not affected. After the larger load, VGX significantly reduced Fos-ir in the parvocellular PVN and in the NTS, but not in the other regions. Thus, decreased water intake by VGX rats was accompanied by decreased Fos-ir in the parvocellular PVN after the same treatments, indicating a role for the abdominal vagus in thirst in response to signaling from gut osmoreceptors. The decreased water intake in the VGX group was not reflected as a decrease in Fos-ir in the SFO. Absorption of the larger i.g. load may have activated Fos-ir through more rapidly increasing systemic osmolality, thereby obscuring a role for the vagus at this dose in the SON and magnocellular PVN.

Animals↗
PubMed1976

Recurrent hypernatremia; a proposed mechanism in a patient with absence of thirst and abnormal excretion of water.

A 7-year-old girl twice developed severe hypernatremia (serum sodium values up to 194 mEq/l) without obvious cause. The ability of her kidneys to conserve water was normal, and increasing her plasma osmolality stimulated an appropriate ADH response. Unable to excrete a water load, her kidneys continued to conserve water even with a serum sodium concentration of 133 mEq/l. She was never thirsty and did not ingest sufficient fluid by choice. Although there was no demonstrable anatomic lesion, we postulate a localized defect of her thirst center. This may have modified release of ADH and resulted in an inability to dilute the urine by interrupting a pathway that could exist from the thirst center to the supraoptic nuclei. A therapeutic regimen based on these studies has prevented further hypernatremia.

Child↗
PubMed2003

Thermal dehydration-induced thirst in lithium-treated rats.

Lithium is used as the primary treatment for bipolar disorder but has the common side effects of diuresis and thirst. In the present study, the effects of lithium on water balance responses of male Sprague-Dawley rats to thermal dehydration were examined. Rats ate either unadulterated food or food containing 2 g/kg lithium carbonate for 10 days. Then the control and lithium-treated rats were exposed to either 25 or 37.5 degrees C without food or water for 4 h. The rats were then allowed access to water for 3 h at 25 degrees C or were anesthetized and blood samples were taken. Lithium treatment caused an initial decrease in food intake, a decrease in body weight, and an increase in urine output. Heat exposure caused similar increases in evaporative water loss in control and lithium-treated rats. Heat exposure led to changes in blood indicators of body water status indicative of dehydration, whereas lithium had no effects on blood indicators of body water status. Water intake was increased by both heat exposure and by lithium treatment with the lithium-treated rats being more responsive to the thirst-inducing effects of thermal dehydration. Lithium treatment does not appear to impair water balance responses to heat exposure.

Animals↗
PubMed1998

Perioperative thirst: a patient perspective.

Many institutions continue to require surgery patients to take nothing by mouth after midnight despite current research that supports allowing most patients to drink fluids up to 3 hours before surgery. This study of 50 elective surgery patients describes their perceptions of discomfort caused by thirst. Results show that thirst caused significantly more discomfort to the patient than not being able to eat or sleep or worrying about the surgery itself. Given these results, nurses are urged to work within their institutions to change the current practice regarding preoperative fluid restriction.

Adult↗
PubMed1978

Osmoregulatory thirst in rats after lateral preoptic lesions.

In confirmation of previous observations, lesions of the lateral preoptic area in rats abolished water ingestion during a 4-hr test following an intraperitoneal injection of hypertonic NaCl solution. However, it was observed that these animals increased their water intakes when tests were prolonged to 24 hr and drank almost exactly what they needed for osmoregulation. Furthermore, they increased their water intakes normally when NaCl was given in their diet, when NaCl was administered intravenously, or when they were water deprived and given preloads of isotonic saline to remove hypovolemia. These findings indicate that rats with lateral preoptic lesions do experience osmoregulatory thirst, and consequently, they raise new doubts about whether osmoreceptors located in the lateral preoptic area mediate thirst following the administration of osmotic loads.

Animals↗
PubMed1984

Reduced thirst after water deprivation in healthy elderly men.

To determine whether responses to dehydration are altered with age, we investigated the thirst, fluid and electrolyte responses, and hormonal responses to 24 hours of water deprivation in seven healthy active elderly men (67 to 75 years old) and seven healthy young men (20 to 31 years old) who were matched for weight loss during water deprivation. After water deprivation, the older men had greater increases in plasma osmolality, sodium concentration, and vasopressin levels. However, their urinary osmolality was lower and they were less thirsty and drank less after water deprivation, so that their plasma and urine were not diluted to predeprivation levels. Regression analysis indicated increased sensitivity of vasopressin osmoreceptors in the older group, although this difference was not statistically significant. We conclude that after 24 hours of water deprivation, there is a deficit in thirst and water intake in healthy elderly men, as compared with younger men, although vasopressin osmoreceptor responsiveness is maintained or even increased. Our findings also suggest that the well-known deficit in urinary concentrating ability that occurs with age reflects renal causes and not a lack of circulating vasopressin.

Adult↗
PubMed1977

Increased thirst and hunger in adult rats undernourished as infants: an alternative explanation.

1. Rats were undernourished in early life by feeding their mothers a restricted quantity of a good-quality diet throughout lactation. Their undernutrition continued postweaning from 25 to 42 d of age, after which they were fed ad lib. Control rats were well nourished at all times. 2. Behavioural assessment of thirst was carried out on adult males. These were deprived of water for 23 h/d throughout the period of testing. Compared to control rats, previously-undernourished (PU) rats pressed a lever at a higher rate in a Skinner box to gain a water reward, drank more frequently during their first 5 min in an unfamiliar cage, and tended to run more quickly down an alleyway for water. PU rats also drank more (/kg body-weight 0-75) of a quinine solution (I g/l) when this was available to them ad lib. as their only source of fluid. 3. A second group of rats was growth-retarded during gestation and the suckling and early postweaning periods. The rats had free access to food from 42 d of age. In adulthood their ad lib. food and water consumption was measured. PU males ate and drank more (/kg body-weight 0-75) than control males. 4. These results indicate that adult rats which have been undernourished in early life display increased thirst. An attempt is made to explain this finding, together with their previously-demonstrated enhanced hunger drive, purely in terms of gross anatomical and physiological differences.

Animals↗
PubMed1976

Establishment of a secondary drive based on thirst: a replication.

In order to establish a secondary drive based on thirst, 16 male albino rats were deprived of water for 23 hours per day for 14 days in square cages. At the end of each 23-hour period, the Ss were placed in triangular cages with free access to water for 1/2 hour followed by 1/2 hour in a circular cage with no water available. On day 15 the Ss were divided into two groups following satiation in the triangular cage. The control Ss were placed in the circular cages with water present for the first time, and experimental Ss were placed in the square cages with water present for the first time. During this 1/2-hour period the experimental Ss drank significantly more than the control Ss which indicated the presence of thirst fear in the experimental group.

Animals↗
PubMed1980

Conditioned thirst in rats.

The purpose of these studies was to assess the appropriateness of control groups in previous thirst conditining studies and to demonstrate that conditioned drinking can be viewed as a classically conditioned appetitive response. In Experiment I (N = 48) thirst was conditioned by the procedure employed by Solomon and Swanson [see Mowrer (11)]. With the use of a "novel cage" group, suppression rather than enhancement of intake was obtained. These and other investigators' results were interpreted in the light of the appropriateness of control groups. In Experiment II (N = 30) rate demonstrated increased water intake at zero hours water deprivation in the presence of an external stimulus previously paired with an increasing motive state. Intakes monitored at half-hour intervals revealed that "low-to-high" drive associated stimuli did not affect overall intake but did induce differentiation in drinking patterns causing first enhancement and then reduction in intake amounts. The results were agreement with Seligman et al. (14) who suggested that elicitation of the prepared mechanism evokes drinking, but water regulation controls do not allow prolonged hyperdipsia.

Animals↗
PubMed2004

Reduced thirst in patients with a vasospastic syndrome.

PURPOSE: To compare thirst, drinking behaviour, and endothelin-1 (ET-1) plasma levels between vasospastic and non-vasospastic subjects. METHODS: We compared 67 subjects with a primary vasospastic syndrome with 64 age- and sex-matched non-vasospastic control subjects. A detailed medical history was recorded, including a questionnaire containing queries about thirst and drinking behaviour, history of migraine or unspecific headache, history of episodes of low blood pressure, and smoking habits. Body mass index (BMI) was calculated and blood samples were drawn for ET-1 measurements. RESULTS: Subjects with a vasospastic syndrome reported a reduced desire to drink and a lower estimated quantity of daily fluid intake, more often forgot to drink, more often had both migraine and unspecific headache, more often had episodes of low blood pressure, and had an increased plasma level of ET-1. These features differed statistically significantly between the two groups. There was also a non-significant trend among vasospastic subjects to smoke less and to have a smaller BMI. CONCLUSION: A reduced desire to drink is found frequently among vasospastic subjects.

Adult↗
PubMed1990

Aging and disturbances of thirst and fluid balance.

Fluid and electrolyte homeostasis depend on a balance between the intake and output of water. Aging is characterized by reduced homeostatic capacity. Changes in the control of both water intake and excretion accompany aging and may predispose the elderly to disturbances in sodium and water balance. Reduced thirst and water intake in response to water deprivation and thermal dehydration have been observed in healthy elderly persons. This reduction, combined with reduced renal water-conservation capacity, may predispose the elderly to dangerous dehydration when illness increases water losses or physical incapacity prevents access to water. The reasons for the thirst deficit are not clear. The elderly have a reduced capacity to excrete a water load, which means they are predisposed to water overload and hyponatremia. Furthermore, various neuroendocrine changes in the elderly affect fluid and electrolyte homeostasis. More studies are needed to understand the etiology of the disturbances of fluid intake and output so that they can be better prevented and treated.

Aging↗
PubMed1984

Increased or decreased thirst caused by inhibition of angiotensin-converting enzyme in the rat.

We have investigated the effects on water intake of subcutaneous (S.C.) injections of low (0.5 mg/kg) and high (100 mg/kg) doses of captopril, an inhibitor of angiotensin-converting enzyme (CE). Low doses block the synthesis of angiotensin II only in the circulation whereas high doses block CE in both the blood and the brain. The low dose of captopril enhanced drinking in response to three hypotensive drugs, isoprenaline (0.1 mg/kg, S.C.), phentolamine (5 mg/kg, S.C.) and serotonin (2 mg/kg, S.C.), whereas the high dose of captopril abolished drinking in response to these stimuli. The low dose of captopril also enhanced drinking in response to histamine (0.25-5.0 mg/kg, intraperitoneal, I.P.), but in this case the high dose of captopril only partially reduced the drinking response. The low dose of captopril enhanced drinking after 24 h water deprivation but high doses had no significant effect on deprivation-induced thirst. Hypovolaemia was produced either by injecting polyethylene glycol (30% w/v, 10 ml/kg) S.C. or by replenishing the cellular deficit in water-deprived rats with 10 ml water (by gavage). The low dose of captopril enhanced the drinking response to hypovolaemia but the high dose had no significant effect. Neither the high nor the low dose of captopril significantly affected drinking in response to cellular dehydration caused by injecting 2 M-NaCl (2 ml) I.P. or by replenishing the extracellular deficit in water-deprived rats (10 ml balanced salt solution by gavage). Nephrectomy (but not ligation of the ureters) or injections of propranolol (5 mg/kg, S.C.) to prevent renin secretion prevented the enhancement of deprivation-or serotonin-induced thirst by the low dose of captopril. The low dose of captopril did not enhance drinking in response to I.V. injections of renin (1 Goldblatt unit), or intracerebroventricular (I.C.V.) injections of angiotensin I or II. The high dose of captopril blocked drinking in response to I.V. injections of renin or I.C.V. injections of angiotensin I but did not reduce drinking in response to angiotensin II, I.C.V. These results are consistent with the hypothesis that blocking CE only in the circulation enhances drinking in response to hypotension or hypovolaemia because angiotensin I, accumulating in high concentration in the blood, enters the brain and is converted intracerebrally to angiotensin II. These findings suggest that the enhancement of drinking caused by low doses of captopril s.c. is a sensitive indicator of whether the renin- angiotensin system participates at all in the regulatory response to a particular stimulus to drink.(ABSTRACT TRUNCATED AT 400 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1973

Renin-angiotensin role in thirst: paradoxical enhancement of drinking by angiotensin converting enzyme inhibitor.

A competitive angiotensin converting enzyme antagonist SQ 20, 881 (SQ), was used to examine the role of the renin-angiotensin system in putative renin-dependent thirst in the albino rat. Significant enhancement of "renin-dependent" as well as renin-independent drinking was observed in the presence of peripheral SQ. Intraventricular SQ obviated this enhancement of drinking but did not affect the water intake caused by the original stimulus itself, whereas it sharply reduced drinking evoked by peripheral renin in nephrectomized rats. Prior renin depletion likewise had no influence on so-called renin-dependent thirst.

Angiotensin II↗
PubMed1992

Investigating the role of angiotensin II in thirst: interactions between arterial pressure and the control of drinking.

Several lines of evidence suggest that angiotensin II plays a physiological role in the control of thirst. Establishing that, however, has been surprisingly difficult, given our current knowledge about the renin-angiotensin systems in the circulation and the brain and the variety of techniques available to measure and manipulate them. A major problem is that stimulating or blocking the renin-angiotensin system affects several physiological variables simultaneously. Since several of these variables also influence the controls of water intake directly or indirectly, the interpretation of the effect on drinking becomes more difficult. To illustrate the problem and recent developments, this paper describes some of the interactions between the effects of angiotensin II on arterial pressure and thirst, and it shows how they have contributed to the controversy over the physiological role of the peptide.

Angiotensin II↗
PubMed1975

Localization of thirst and antidiuretic osmoreceptors by intracranial injections in rats.

Eighty-six intracranial cannula placements in 51 rats were tested with unilateral, 2-mul injections of a 0.60-osmol/kg solution, sucrose dissolved in isotonic sodium chloride. To assess antidiuretic hormone (ADH) release, a water diuresis was induced and spontaneous urinations were collected and analyzed for sodium by flame photometry. On alternate test days the 0.60-osmol/kg solution was injected into sleeping rats, and latencies to drink and volume drunk were recorded. Injections at 42 placements elicited neither drinking nor adtidiuresis on two separate test days each; at 15, both antidiuresis and drinking on at least two of three tests each; at 19, drinking but not antidiuresis; at 10, antidiuresis but not drinking. Positive drinking and ADH placements were not distinctly separated. They clustered in the bed nucleus of the stria terminalis, the preoptic areas, and the anterior portions of the hypothalamus. Placements in the medial forebrain bundle and dorsal to the anterior hypothalamic area elicited thirst but not ADH release for the most part. Placements nearest the supraoptic nucleus were weak or negative for ADH release. Central nervous system osmo-receptors exist and seem not to be the neurosecretorycells. Thirst osmoreceptors and antidiuretic osmoreceptors seem to be contiguous, but distinct.

Angiotensin II↗
PubMed1976

Effect of prolonged angiotensin II infusion on thirst.

To determine the effect of prolonged angiotensin II (A-II) infusion on thirst, daily water intake by drinking was measured in dogs during a 4-day control period, a 4-day period of vehicle infusion without A-II, a 10-day period of A-II infusion, and a 4-day recovery period of vehicle infusion without A-II. During the control period and the periods of vehicle infusion in the absence of A-II, daily water intake by drinking in four dogs averaged 118 +/- 20 ml/day (mean +/- SE). During the 10-day period of A-II infusion at the rate of 13.0 ng/kg per min drinking increased to 269 +/- 49 ml/day (paired t; P less than 0.05). Angiotensin II infusion at the rate of 26.0 ng/kg per min produced a sustained increase in water intake in two dogs during an 8-day period of infusion. These results demonstrate that in dogs, prolonged infusion of angiotensin II stimulates the thirst mechanism and that the effect lasts for more than a few days.

Aldosterone↗
PubMed2002

Early osmoregulatory stimulation of neurohypophyseal hormone secretion and thirst after gastric NaCl loads.

Cerebral osmoreceptors mediate thirst and neurohypophyseal secretion stimulated by increases in the effective osmolality of plasma (P(osmol)). The present experiments determined whether an intragastric load of hypertonic saline (ig HS; 0.5 M NaCl, 4 ml) would potentiate these responses before induced increases in P(osmol) in the general circulation could be detected by cerebral osmoreceptors. Adult rats deprived of water overnight and then given intragastric HS consumed much more water in 15-30 min than rats given either pretreatment alone, even though systemic P(osmol) had not yet increased significantly because of the gastric load. In other rats pretreated with an intravenous infusion of 1 M NaCl (2 ml/h for 2 h), plasma levels of vasopressin and oxytocin were considerably elevated 15 and 25 min after intragastric HS treatment, whereas systemic P(osmol) was not increased further. These and other findings are consistent with previous reports that hepatic portal osmoreceptors (or Na(+) receptors) stimulate thirst and neurohypophyseal hormone secretion in euhydrated rats given gastric NaCl loads and indicate that these effects are potentiated when animals are dehydrated.

Animals↗
PubMed2007

Presystemic influences on thirst, salt appetite, and vasopressin secretion in the hypovolemic rat.

The present studies investigated the influence of presystemic signals on the control of thirst, salt appetite, and vasopressin (VP) secretion in rats during nonhypotensive hypovolemia. Rats were injected with 30% polyethylene glycol (PEG) solution, deprived of food and water overnight, and then allowed to drink water, 0.15 M NaCl, or 0.30 M NaCl. The PEG treatment, which produced 30-40% plasma volume deficits, elicited rapid intakes in an initial bout of drinking, but rats consumed much more 0.15 M NaCl than water or 0.30 M NaCl. In considering why drinking stopped sooner when water or concentrated saline was ingested, it seemed relevant that little or no change in systemic plasma Na(+) concentration was observed during the initial bouts and that the partial repair of hypovolemia was comparable, regardless of which fluid was consumed. In rats that drank 0.15 M NaCl, gastric emptying was fastest and the combined volume of ingested fluid in the stomach and small intestine was largest. These and other observations are consistent with the hypothesis that fluid ingestion by hypovolemic rats is inhibited by distension of the stomach and proximal small intestine and that movement of dilute or concentrated fluid into the small intestine provides another presystemic signal that inhibits thirst or salt appetite, respectively. On the other hand, an early effect of water or saline consumption on VP secretion in PEG-treated rats was not observed, in contrast to recent findings in dehydrated rats. Thus the controls of fluid ingestion and VP secretion are similar but not identical during hypovolemia.

Animals↗