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PubMed1980

Thirst and vasopressin release in the dog: an osmoreceptor or sodium receptor mechanism?

The effects of intravenous infusion of hypertonic NaCl, sucrose, glucose, urea, or isotonic NaCl solution on thirst and plasma arginine vasopressin concentration (AVP) were studied in five conscious dogs. The changes in osmolality and sodium concentration of plasma and cerebrospinal fluid (CSF) were measured at the threshold of drinking, or after 45 min if no drinking occurred. Hypertonic NaCl and sucrose stimulated drinking in all dogs and significantly elevated plasma AVP. Equally hypertonic glucose, urea, or isotonic NaCl failed to stimulate any drinking or vasopressin secretion. All hypertonic solutions caused significant and similar increases in the osmolality and sodium concentration of CSF. Plasma osmolality was increased by the hypertonic solutions. Plasma sodium was increased by hypertonic NaCl, decreased by sucrose and glucose, and not changed by urea. Isotonic NaCl had no effect on either plasma or CSF composition. These data are not consistent with either a sodium or an osmoreceptor mechanism located within the blood-brain barrier (BBB) or with a peripheral sodium receptor mechanism. An intracranial osmoreceptor located on the blood side of the BBB is proposed to explain these results.

Animals↗
PubMed1988

Angiotensin-related sodium appetite and thirst in cattle.

Cows depleted of Na by loss of saliva from a parotid fistula for 46 h had an avid appetite for Na solution. They drank 21.0 +/- 1.6 liter of 0.3 M NaHCO3-NaCl solution during 2 h of access but little or no water during that time. Solutions of angiotensin II or captopril were infused for 3 h intravenously or into a lateral ventricle (intracerebroventricular) beginning 1 h before access to Na solution. Intravenous angiotensin II increased Na intake (to 26.8 +/- 2.9 liter, P less than 0.01) but did not alter water intake. Intracerebroventricular angiotensin II increased water intake but did not alter Na intake. Intravenous captopril reduced Na intake (to 11.0 +/- 2.1 liter, P less than 0.001) and concurrent intravenous angiotensin II prevented the reduction but concurrent intracerebroventricular angiotensin II did not. Intracerebroventricular captopril did not alter Na or water intake. Intravenous captopril reduced to zero the water intake during the hour before Na access, and concurrent intravenous angiotensin II prevented that reduction also. The dipsogenic action of intracerebroventricular angiotensin II was potentiated by intravenous captopril. The results of these experiments suggest that if angiotensin II receptors involved in the mechanism regulating Na appetite are in the brain, they are accessible only from the blood, e.g., in circumventricular organs. Thirst was inhibited by reduction of angiotensin II in blood but was stimulated only by angiotensin II acting inside the blood-brain barrier.

Angiotensin II↗
PubMed1989

Osmoregulation of vasopressin secretion and thirst during the estrous cycle of pigs.

The influence of the reproductive cycle on ingestive behaviors, osmotically induced fluid intake, and peripheral blood levels of several hormones involved in fluid electrolyte balance was investigated in young adult female pigs. Food, water, and salt intakes and plasma aldosterone levels were significantly lower during estrus compared with the luteal and follicular phases, whereas plasma sodium (PNa) was higher. Plasma renin activity and lysine vasopressin (LVP) levels did not vary with the cycle. Regression analyses of the relationship between plasma LVP and PNa in unanesthetized, unstressed animals infused for 2 h with intravenous 5% NaCl revealed no significant differences in terms of the osmotic threshold and sensitivity of LVP release at different stages of the reproductive cycle. In contrast, when osmotic loading was carried out with continuous access to water, the osmotic threshold for drinking was found to be significantly higher and the rate of drinking lower during estrus. The results indicate that in the adult female pig the stage of the reproductive cycle has an influence on ingestive behaviors and the osmoregulation of thirst. Osmoregulation of vasopressin secretion, on the other hand, appears to be independent of the estrous cycle in this species.

Animals↗
PubMed1991

Effect of atrial natriuretic peptide on thirst and arginine vasopressin release in humans.

We investigated the effect of human alpha-atrial natriuretic peptide (alpha-hANP) on osmotically stimulated arginine vasopressin (AVP) secretion and thirst appreciation. Seven normal male volunteers were studied on two occasions: synthetic alpha-hANP-(99-126) (2 pmol.kg-1.min-1) or control was infused intravenously for 30 min before and for the first 60 min of a 120-min hypertonic saline (855 mmol/l) infusion (0.06 ml.kg-1.min-1). Plasma ANP did not alter significantly during infusion of control and hypertonic saline (C+HS) but rose to steady-state concentrations of 17.4 +/- 3.2 pmol/l during infusion of ANP and hypertonic saline (ANP+HS). Plasma osmolality increased on both study days [ANP+HS: 284.4 +/- 0.6 to 299.7 +/- 1.1 mosmol/kgH2O (P less than 0.01)], C+HS: 283.6 +/- 1.2 to 299.1 +/- 1.6 mosmol/kgH2O (P less than 0.01)], as did plasma sodium [ANP+HS: 139.0 +/- 0.6 to 148.0 +/- 0.4 mmol/l (P less than 0.01), C+HS: 137.6 +/- 0.75 to 145.8 +/- 0.7 mmol/l (P less than 0.01)] and blood volume (ANP+HS: 7.7 +/- 0.6%, C+HS: 9.4 +/- 1.0%). The increase in plasma osmolality was accompanied by an increase in plasma AVP [ANP+HS: 1.4 +/- 0.3 to 8.3 +/- 1.2 pmol/l (P less than 0.01), C+HS: 1.6 +/- 0.4 to 7.8 +/- 1.5 pmol/l (P less than 0.01)].(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Thirst and brain angiotensin in cattle.

Cows that were normally hydrated or deprived of water were given intravenous or intracerebroventricular (icv) infusions of angiotensin I converting-enzyme inhibitors (CEI) or angiotensin II antagonists. Normally hydrated Na-deficient cows increased water intake in a dose-related manner in response to icv infusion of angiotensin I (n = 5). The response to 3 micrograms/h angiotensin I was abolished by concurrent icv infusion of the CEI captopril at 3 mg/h but not by intravenous infusion of captopril at 120 mg/h, which reduced Na appetite (n = 5). The icv infusion of captopril at 12 mg/h did not reduce the water intake of cows that were water restricted for 26.5 h (n = 4) or water restricted and Na deficient (n = 4). The icv infusion of the more lipophilic CEI ramipril at 3 mg/h (n = 7) did not reduce the water intake of normally hydrated or dehydrated cows but reduced the "need-free" intake of Na solution by dehydrated cows. The icv infusion of the nonpeptide antagonist Du Pont 753 at 3 mg/h (n = 7) reduced water intake in dehydrated cows. The results indicate that brain angiotensin may be involved in thirst in cattle. The data suggest that this brain angiotensin II may be formed by a pathway that does not include converting enzyme and that is sited inside the blood brain barrier, possibly in the median preoptic nucleus.

Angiotensin I↗
PubMed1995

Thermal dehydration-induced thirst in rats: role of body temperature.

Male Sprague-Dawley rats were used to study the possible role of hyperthermia in the thirst associated with thermal dehydration. Rats were exposed to 40 degrees C for 4 h and then allowed access to water at different times after they were transferred to 25 degrees C. Delaying the time prior to allowing the rats to drink did not significantly alter either water intake or percent rehydration even though core temperature decreased during the first 1.5 h after removal from the heat. Exposing thermally dehydrated rats to 5 degrees C for 30 min prior to allowing them access to water also failed to significantly affect water intake or percent rehydration. Thermally dehydrated rats allowed to drink while remaining in the heat did not show a significant increase in water intake during the first hour or percent rehydration over rats drinking at 25 degrees C. Nondehydrated rats did show significant increases in water intake and percent rehydration when allowed to drink in the heat. Hyperthermia does not play a role in drinking in thermally dehydrated rats but can stimulate drinking in water-replete rats.

Animals↗
PubMed1997

Central infusion of the AT1 receptor antagonist losartan inhibits thirst but not sodium appetite in cattle.

Experiments in cattle compared the effects of intracerebroventricular (i.c.v.) infusions of losartan and PD-123319 on water intake caused by water restriction, i.c.v. infusion of hypertonic NaCl, or i.c.v. infusion of angiotensin II (ANG II). The effects of these receptor antagonists on sodium intake caused by sodium depletion were also examined. Losartan infusion caused dose-dependent inhibition of the high water intake caused by the physiological stimulus of water restriction or by ANG II infusion but did not affect salt appetite. PD-123319 infused at equimolar or greater (in ANG II experiments) doses did not affect water intake or salt intake due to sodium depletion. The results of these i.c.v. infusion experiments confirm our earlier proposal that the physiological regulation of water intake in cattle may be mediated by ANG II acting centrally via AT1 receptors. The dose of losartan that inhibited thirst in cattle did not inhibit sodium appetite, nor did an equimolar dose of PD-123319.

Angiotensin II↗
PubMed1999

Effects of subfornical organ lesions on acutely induced thirst and salt appetite.

We examined the role of the subfornical organ (SFO) in stimulating thirst and salt appetite using two procedures that initiate water and sodium ingestion within 1-2 h of extracellular fluid depletion. The first procedure used injections of a diuretic (furosemide, 10 mg/kg sc) and a vasodilator (minoxidil, 1-3 mg/kg ia) to produce hypotension concurrently with hypovolemia. The resulting water and sodium intakes were inhibited by intravenous administration of ANG II receptor antagonist (sarthran, 8 micrograms . kg(-1). min(-1)) or angiotensin-converting enzyme inhibitor (captopril, 2.5 mg/h). The second procedure used injections of furosemide (10 mg/kg sc) and a low dose of captopril (5 mg/kg sc) to initiate water and sodium ingestion upon formation of ANG II in the brain. Electrolytic lesions of the SFO greatly reduced the water intakes, and nearly abolished the sodium intakes, produced by these relatively acute treatments. These results contrast with earlier findings showing little effect of SFO lesions on sodium ingestion after longer-term extracellular fluid depletion.

Angiotensin II↗
PubMed2000

Role of renin-angiotensin system in hypotension-evoked thirst: studies with hydralazine.

Injection of rats either with diazoxide (25 mg/kg iv), isoproterenol (0.33 mg/kg sc), or hydralazine (HDZ) (10 mg/kg ip) decreased arterial blood pressure from approximately 120 to 70-80 mmHg and stimulated renin secretion. However, diazoxide and isoproterenol treatments each stimulated water ingestion, whereas HDZ treatment did not. HDZ treatment did not reduce water intake evoked by systemic injection of hypertonic saline or 20% polyethylene glycol solution or by 24-h water deprivation, suggesting that HDZ treatment did not interfere with drinking behavior. In contrast, HDZ treatment markedly reduced water intake evoked by injection of diazoxide or isoproterenol or by intravenous infusion of renin. Furthermore, a highly significant correlation was observed when plasma ANG II levels were plotted as a function of plasma renin activity after intravenous infusion of renin and after diazoxide and isoproterenol treatments. However, values obtained after HDZ treatment alone or in combination with intravenous infusion of renin did not fall near the 99% confidence interval of the regression line, suggesting that HDZ treatment blocks ANG II production and/or promotes its clearance. Thus rats apparently do not increase water intake after HDZ treatment, because this drug interferes with the renin-angiotensin system. These results provide further evidence that arterial hypotension evokes thirst in rats predominantly by activation of the renin-angiotensin system.

Animals↗
PubMed2004

Evidence for bradykinin as a stimulator of thirst.

Angiotensin-converting enzyme inhibition (ACEI) with captopril has been shown to increase water intake and urine output in rats, but the mechanism is unknown. ACEI impairs the conversion of ANG I to ANG II, a dipsogenic hormone, and impairs the degradation of bradykinin. The goal of this study was to examine the role of bradykinin in the polydipsia and polyuria associated with ACEI. Male Sprague-Dawley rats received captopril (CPT; 20 mg.kg(-1).day(-1)) in ground chow for 48 h. Water intake, food intake, and urine output were monitored and compared with control rats (CTL), rats receiving captopril treatment with limited water intake (CPT-LIM), and rats receiving captopril treatment with ad libitum water intake plus 24-h treatment with the bradykinin antagonist B-9430 (CPT-BK1). CPT rats consumed significantly more water and produced more urine vs. CTL. Urine osmolality was significantly decreased in CPT rats vs. CTL. Inner medullary aquaporin-2 (AQP2) protein abundance was also markedly decreased in CPT rats vs. CTL. These findings were reversed in CPT-LIM rats, suggesting captopril-induced primary polydipsia. CPT-BKI rats demonstrated parameters no different from CTL despite ad libitum water intake. Mean arterial pressure and 24-h creatinine clearance did not differ among groups. We conclude that ACEI with captopril induces primary polydipsia despite impaired production of the dipsogen ANG II and that this primary increase in water intake is likely the cause of the decreased protein abundance of inner medullary AQP2. Furthermore, this dipsogenic effect was reversed by antagonism of bradykinin, thus implicating this hormone in thirst regulation in the rat.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1984

Altered osmotic thresholds for vasopressin secretion and thirst in human pregnancy.

Osmoregulation was studied in eight women during late pregnancy and again 8-10 wk postpartum. Base-line plasma osmolality (Posmol) was significantly lower during (280.9 +/- 2.1 mosmol/kg, SD) than after (289.4 +/- 2.1 mosmol/kg) pregnancy yet 24-h urinary volume and plasma arginine vasopressin (PAVP) measured in vasopressinase-inactivated blood was similar in both groups (pregnancy, 1.39 +/- 0.56 pg/ml; postpartum, 1.25 +/- 0.62 pg/ml). After 12 h of dehydration PAVP rose similarly and significantly both during (2.25 +/- 0.81 pg/ml) and after (2.89 +/- 1.19 pg/ml) gestation, and Uosmol was similar on both occasions (pregnancy, 779 +/- 121 mosmol/kg; postpartum, 784 +/- 102 mosmol/kg). When Posmol was increased by the slow infusion of 5% saline PAVP increased as soon as body tonicity did both during and after pregnancy. PAVP correlated significantly with Posmol in each subject (range of r, 0.75-0.99) and the mean regression lines [pregnancy, PAVP = 0.32 (Posmol; -279), r = 0.79; postpartum, PAVP = 0.38 (Posmol, -285), r = 0.86] demonstrated that the apparent osmotic threshold for AVP secretion was 6 mosmol/kg lower during than after gestation. Similarly the Posmol at which the subject experienced a conscious desire to drink was lower in pregnant (287 +/- 1.6 mosmol/kg) compared with postpartum subjects (298 +/- 2.0 mosmol/kg; P less than 0.001). These data demonstrate decreased osmotic thresholds for AVP release and thirst during human pregnancy and explain why gravidas can maintain their new lower Posmol within narrow limits.

Adult↗
PubMed2003

Human cortical responses to water in the mouth, and the effects of thirst.

In an event-related functional magnetic resonance imaging (fMRI) study in humans it was shown, first, that water produces activations in cortical taste areas (in particular the frontal operculum/anterior insula which is the primate primary taste cortex, and the caudal orbitofrontal/secondary taste cortex) comparable to those produced by the prototypical tastants salt and glucose. Second, the activations in the frontal operculum/anterior insula produced by water when thirsty were still as large after the subjects had consumed water to satiety. Third, in contrast, the responses to water in the caudal orbitofrontal cortex were modulated by the physiological state of the body, in that responses to the oral delivery of water in this region were not found after the subjects had drunk water to satiety. Fourth, further evidence that the reward value or pleasantness of water is represented in the orbitofrontal cortex was that a positive correlation with the subjective ratings of the pleasantness of the water was found with activations in the caudal and anterior orbitofrontal cortex, and also in the anterior cingulate cortex. Fifth, it was found that a region of the middle part of the insula was also activated by water in the mouth, and further, that this activation only occurred when thirsty. Sixth, analyses comparing pre- and postsatiety periods (i.e., when thirsty and when not thirsty) independently of stimulus delivery revealed higher activity levels in the rostral anterior cingulate cortex. The activity of the rostral anterior cingulate cortex thus appears to reflect the thirst level or motivational state of the subjects.

Cerebral Cortex↗
PubMed1996

Quenching the thirst in dialysis patients.

In a double-blind cross-over trial, 22 stable end-stage renal failure patients on maintenance haemodialysis were subjected to conventional dialysis with dialysate containing 137 mEq/l sodium and constant ultrafiltration (UF) and to a different dialysis therapy, in which, by linear sodium modelling, the dialysate sodium was reduced from 137 to 128 mEq/l. A computerized UF program was used to gradually reduce the UF to a minimum towards the end of the session. Severity of thirst, interdialytic weight gain and intradialytic complications were less with low sodium dialysate. It allowed adequate UF with absolute hemodynamic stability. The reduced incidence of complication with low sodium dialysate therapy was probably because they required less UF.

Adult↗
PubMed2006

Pilocarpine-induced salivation and thirst in conscious rats.

The muscarinic receptor agonist pilocarpine is widely used as a sialogogue. It has been well-established that it also induces water intake in animals. However, the mechanisms underlying the relationships between these events are unknown. To address this problem, we examined water intake and parotid salivary secretion in conscious rats. Intraperitoneally injected pilocarpine increased both water intake and salivary secretion. Intracerebroventricularly injected pilocarpine also induced water intake, but not salivary secretion. Intracerebroventricularly applied atropine, a muscarinic receptor antagonist, suppressed the water intake produced by pilocarpine applied intraperitoneally and intracerebroventricularly. However, it did not affect the salivary secretion induced by pilocarpine applied peripherally. We conclude that peripherally applied pilocarpine affects the parotid glands and the thirst center in the central nervous system, while it may induce salivary secretion mainly via peripheral responses, but water intake mainly via the central nervous system.

Animals↗
PubMed1991

Drinking, thirst and water intoxication.

Drinking is an activity determined partly by oropharyngeal stimulation and gastrointestinal sensations as well as biochemical changes, and thirst need not be involved. It is sometimes disturbed in mania or depression. Overdrinking (polydipsia) is common in long-stay in-patients, but only gives rise to water intoxication when there is a variable functional renal abnormality such as SIADH causing water retention. In contrast, in affective disorders, disturbance of sodium retention may be seen, possibly representing failure of nervous vascular control as part of the mental illness.

Bipolar Disorder↗
PubMed1990

Roles of peripheral and central angiotensin-converting enzyme (ACE) in hypovolemic thirst induced by compound 48/80 in rats.

Subcutaneous (s.c.) injection of Hoe 498, an angiotensin converting enzyme (ACE) inhibitor, at the doses of 0.1, 0.5, 1.0 and 4.0 mg/kg produced a dose-related inhibition of compound 48/80-induced hypovolemic thirst in rats. A significant time-response relationship was observed between the pretreatment time of Hoe 498 at a dose of 4.0 mg/kg and the inhibition of compound 48/80-induced water intake. Nearly 90% of plasma ACE activity was inhibited by Hoe 498 at all doses used, and this inhibition at the dose of 4.0 mg/kg of Hoe 498 continued for more than 4 hr. Intracerebroventricular (i.c.v.) or s.c. injection of Hoe 498 in doses ranging from 0.5 to 20 micrograms comparably inhibited plasma ACE activity in a dose-dependent manner. The compound 48/80-induced water intake was significantly reduced by i.c.v. injection of Hoe 498 (20 micrograms) 30 min after compound 48/80 administration, but not reduced when the drug was given 15 min prior to injection of dipsogen. The inhibition of water intake by Hoe 498 seems to be dependent on the dose and time between administration of Hoe 498 and compound 48/80. The present data suggest that brain ACE is more involved in compound 48/80-induced water intake than peripheral systemic ACE.

Angiotensin II↗
PubMed1984

Localization of central nervous system structures mediating extracellular thirst in the female rat.

Water intake elicited by microinjection of the hormone angiotensin-II into the preoptic region of cyclic female rats was significantly less on days of vaginal oestrus than at dioestrus or metoestrus, whereas the drinking of 2.7% NaCl solution, to which rats also had access, did not vary with the cycle. Administration of the same dose of angiotensin-II to the subfornical organ and the lateral cerebral ventricles induced drinking at all stages of the oestrous cycle, but the volumes of water or 2.7% NaCl ingested did not vary with the cycle. Water intake after subcutaneous injection of isoprenaline, a beta-adrenergic agonist which causes increased angiotensin biosynthesis, varied cyclically with the stage of the oestrous cycle. On the other hand, water and 2.7% NaCl intakes induced by intraperitoneal injection of hypertonic NaCl (a cellular stimulus of thirst) or by 24-h water deprivation (which dehydrates both the extracellular and cellular body fluid compartments) did not differ significantly at the various stages of the oestrous cycle. The finding that fluctuations in angiotensin- and isoprenaline-induced water intake parallel the changes in spontaneous 24-h drinking suggests that the preoptic region may play an important role in the maintenance of extracellular fluid balance in synchrony with the oestrous cycle.

Angiotensin II↗
PubMed1987

Sensation of thirst in normal and laryngectomized man.

The purpose of this study was to evaluate the role of the larynx in sensation of thirst and to identify precise areas responsible for the sensation in normal and laryngectomized groups. The present analysis showed that the laryngectomized group was less aware of the sensation and less able to localize it than the normal group. Both groups localized the sensation from the base of the tongue to the larynx as well as in the pharynx.

Adult↗