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PubMed1982

Specific benzodiazepine antagonist RO15-1788 and thirst-induced drinking in the rat.

Midazolam, a new water-soluble benzodiazepine, increased the water intake of water deprived rats. The effect was abolished by concurrent treatment with the benzodiazepine antagonist, RO15-1788. The lack of effect of RO15-1788 on phenobarbitone-induced hyperdipsia confirmed the specificity of the antagonist action. Alone RO15-1788 (0.3-30 mg . kg-1) had no effect on thirst-induced drinking. Thus, it was not necessary to posit the action of an endogenous benzodiazepine ligand in thirst-induced drinking.

Animals↗

PubMed1998

Evidence that brain angiotensin II is involved in both thirst and sodium appetite in baboons.

The roles of ANG II in the brain mechanisms subserving thirst and Na appetite in baboons were investigated by chronic intracerebroventricular infusions of ANG II and AT1-receptor antagonists using subcutaneous miniosmotic pumps and by oral administration of captopril. ANG II at 3 or 5 micrograms/h for 7 days increased water intake from 2,455 +/- 107 to 7,052 +/- 562 ml/day by day 6 and 300 mM NaCl intake from 8.3 +/- 1.1 to 275 +/- 87 mmol/day by day 5. Concurrent intracerebroventricular losartan (300 micrograms/h) did not substantially reduce these responses, but they were abolished by intracerebroventricular ZD-7155 (50 micrograms/h). The increase of 300 mM NaCl intake when it was offered after intramuscular injection of furosemide, 2 mg . kg-1 . day-1 for 3 days, was unaltered by intracerebroventricular losartan (300 micrograms/h) but was reduced by intracerebroventricular ZD-7155 (50 micrograms/h) infused throughout Na depletion/repletion; oral captopril (1 g, 3 and 18 h before access to 300 mM NaCl) also reduced NaCl intake. Restriction of water intake to 25% of daily intake for 3 days caused a high intake of water on day 4, and this was reduced by intracerebroventricular losartan (300 micrograms/h) infused throughout the period of water restriction/rehydration. These novel results in a primate species suggest that brain ANG II is involved in both thirst and Na appetite, acting via AT1 receptors.

Administration, Oral↗

PubMed1975

Dipsogenic effects of intra and extracellular thirst stimuli before and after chronic DFP treatment.

The water intake of rats was observed following subcutaneous administration of intra and extracellular thirst stimuli (hypertonic saline, polyethylene glycol, angiotensin, and isoproterenol) before and after chronic treatment with the anticholinesterase agent, diisopropyl fluorophosphate (DFP), and its arachis oil vehicle. Only hypertonic saline and isoproterenol reliably increased water intake in both groups prior to chronic treatment. After chronic treatment hypertonic saline produced the same degree of water intake in the DFP-treated and control animals, but isoproterenol appeared to produce a greater degree of water intake in the DFP-treated than in the control rats. These results suggest that there are no gross disturbances in the mechanisms underlying intra and extracellular thirst stimuli following the development of tolerance to DFP.

Angiotensin II↗

PubMed1962

Cholinergic tracing of a central neural circuit underlying the thirst drive.

Cholinergic stimulation of any of a number of interrelated limbic and diencephalic structures in the rat elicits a rapid and marked increase in water intake. We postulate that a generalized Papez circuit mediates the thirst drive, that the circuit is specifically and functionally sensitive to cholinergic action, and that other primary drives depend on closely parallel neural circuits partitioned both structurally and biochemically.

Acetylcholine↗

PubMed1995

Central angiotensin II induces thirst-related responses in an amphibian.

Angiotensin II (A-II), a potent inducer of thirst-related behavior in many vertebrate species, was injected into the third ventricle of the brain of the spadefoot toad, Scaphiopus couchii. Following injection of 10 ng A-II the animals demonstrated a significant increase in water absorption response (WR) behavior, in which toads press their ventral skin to a moist surface and absorb water by osmosis. This increase in the frequency of WR behavior was positively correlated with an increase in water gain during a 2-hr period indicating that centrally injected A-II stimulates water intake by this amphibian species. We have previously demonstrated that WR behavior is also induced by intraperitoneal (i.p.) injections of A-II in several anuran species, including S. couchii. Thus, amphibians, like other vertebrates, demonstrate an increase in water intake in response to either centrally administered or circulating A-II. A second series of experiments was conducted to determine whether the above response to A-II might be secondary to increases in the circulating levels of aldosterone (ALDO) or antidiuretic hormone because the release of both of these hormones has been shown by others to be stimulated by A-II. Scaphiopus couchii injected i.p. with either ALDO or arginine vasotocin in dosages of 1, 10, and 100 micrograms/100 g body weight showed no increase in WR behavior relative to toads injected with saline alone. These results suggest that A-II acts directly on the brain of S. couchii to induce WR behavior.

Aldosterone↗

PubMed1975

Equipotency of hypertonic solutions of mannitol and sodium chloride in eliciting thirst in the dog.

The dogs were infused intravenously with either 3.6% NaCl or 20% mannitol solutions. Both infusions stimulated the animals to drink water when similar osmotic loads were introduced and exactly the same degree of cellular dehydration achieved. The amounts of water drunk at thirst threshold did not differ significantly. The results are discussed with relation to the hypothesis of osmometric control of water intake.

Animals↗

PubMed1978

Sex difference in polyethylenglycol-induced thirst.

The polyethylenglycol-induced thirst in male and female castrated rats has been studied. The polyethylenglycol (PG) increases the water intake more in females than in males. Estradiol benzoate and testosterone P. diminishes the amount of water drunk after PG treatment in the females, but not in the males.

Animals↗

PubMed1989

The effect of preoperative apple juice on gastric contents, thirst, and hunger in children.

The effect of 3 ml.kg-1 of apple juice given 2.6 +/- 0.4 hours preoperatively was investigated in 80 healthy children of ages five to ten years in this prospective, randomized, single blind study. The children who drank apple juice preoperatively had decreased gastric volume, thirst, and hunger (p less than 0.05). The gastric volume in the control group was 0.43 +/- 0.46 ml.kg-1 and in the patients who received apple juice the gastric volume was 0.24 +/- 0.31 ml.kg-1. The gastric pH was not significantly different, with the control group's gastric pH being 1.7 +/- 0.6 and the treated group's pH was 2.2 +/- 1.2. Further studies of the effects of different volumes and timing of preoperative clear fluids are indicated in paediatric patients.

Beverages↗

PubMed2004

Water and salt consumption and suppression of Angiotensin-induced thirst in rats after carotid glomectomy.

Carotid glomectomy in rats reduced daily water consumption and increased daily consumption of NaCl solution. Sham operation did not modify water and salt consumption. Intraperitoneal injection of angiotensin-II did not stimulate drinking motivation in the majority of rats subjected to carotid glomectomy. Injection of angiotensin-II to sham-operated and intact animals induced active consumption of both fluids during one hour. These results attest to the involvement of the carotid body in the regulation of consumption of water and sodium ions (the main elements of osmotic blood pressure) and the involvement of angiotensin-sensitive receptors of carotid body cells in the formation of thirst and salt appetite motivation, regulated by the renin-angiotensin system.

Angiotensin II↗

PubMed1979

Idiopathic, sustained, inappropriate secretion of ADH with associated hypertension and thirst.

A 15 year old girl presented with excessive thirst and hypertension (170/110 mm Hg). Biochemical investigations revealed serum sodium 118 meq/liter, serum osmolality 238 mosmol/liter, urine sodium 90 meq/liter, urine osmolality 700 mosmol/liter, persistenly elevated serum antidiuretic hormone (ADH) levels (5.8 to 11.9 pg/ml) and no obvious cause for the hypertension. The hypertension is, at least in part, volume-related, diminishing with fluid restriction. Features of gross water intoxication (e.g., confusion, coma) have not occurred. The etiology of the inappropriate secretion of ADH is not obvious but is not thought to be due to "resetting of osmoreceptors" as evidenced by failure to maximally dilute urine following a water load test and persistently elevated serum ADH levels. A similar patient described by Epstein and associates in 1962 is presently well with persistent features of inappropriate secretion of ADH.

Adolescent↗

PubMed1977

The role of mesencephalic structures in thirst induced by centrally administered angiotensin II.

(1) In 27 animals microinjection of 25--100 ng of angiotensin II through chronic cannulae implanted in the preoptic region initiated drinking and in subsequent acute experiments influenced the spontaneous discharge rate of single neurons in the ipsi-lateral mesencephalon. Of 148 neurons for which recordings were made, 52 (35%) increased their frequency of spike potentials following administration of angiotensin II, 2 (1%) showed inhibition and 94 (64%) showed no change in firing rate. (2) In another series of 44 animals, unilateral or bilateral lesions of the midbrain ventral tegmentum or reticular formation were found to have little or no effect on water intake elicited by the microinjection of angiotensin II into the preoptic region. (3) In contrast to the effects of tegmental and reticular lesions, unilateral lesions located dorsally and laterally to the mammillary peduncle, in the area of passage of the medial forebrain bundle, significantly attenuated the dipsogenic response to either contralateral or ipsilateral injections of angiotensin II into the preoptic region. With bilateral lesions this effect was permanent. (4) Since the more caudal lesions were relatively ineffective in disrupting the elicited drinking, it is suggested that signals from angiotensin II receptors in the preoptic region are transmitted along pathways which diverge in the midbrain. (5) The possibility of a forebrain-hypothalamus-midbrain circuit mediating thirst initiated by activation of the renin-angiotensin system is discussed.

Action Potentials↗

PubMed1992

Amastatin potentiates drinking elicited by osmotic stimuli: evidence for peptidergic mediation of intracellular dehydration-induced thirst.

Aminopeptidase inhibitors have been demonstrated to enhance the behavioral effects of both exogenously applied and endogenously released neuropeptides. In this study peptidase inhibitors were used as probes for involvement of central neuropeptides in osmotically-induced drinking behavior. Intracerebroventricular (i.c.v.) injections of amastatin, an aminopeptidase A inhibitor, potentiated water intake induced by subcutaneous injections of hypertonic saline. Drinking responses to i.c.v. infusions of hypertonic saline were also enhanced when amastatin was added to the infusions. The effect was not attenuated by the angiotensin receptor antagonist, [Sar1, Thr8]angiotensin II, which suggests that angiotensins do not play a role in the over-drinking. Drinking responses to centrally infused hypertonic saline were not enhanced by i.c.v. thiorphan, an endopeptidase inhibitor; this provides evidence that the effects of amastatin are specific for a particular class of peptidases. These results suggest that there is a role for an endogenous, non-angiotensinergic brain peptide in the mediation of osmotic thirst.

Aminopeptidases↗

PubMed1986

Cerebral renin-angiotensin mediation of isoproterenol-induced thirst in the dog.

Pretreatment of dogs with s.c. isoproterenol (10 micrograms/kg) caused a significant increase in drinking when 100 ng renin substrate was administered 3 min later to the lateral cerebral ventricles or subfornical organ. Isoproterenol itself was a potent peripheral (10 micrograms/kg), but unreliable central (0.01-1 microgram) dipsogen. The increased drinking after combined s.c. isoproterenol and intracerebroventricular (i.c.v.) renin substrate injections was significantly attenuated by i.c.v. captopril (20 micrograms), but was not influenced by s.c. captopril (500 micrograms/kg). However, combined i.c.v./s.c. pretreatment with captopril nearly abolished drinking to peripheral isoproterenol, or the combination of s.c. isoproterenol and i.c.v. renin substrate. Finally, single intracranial injections of the components of the renin-angiotensin system elicited dose-dependent and site-specific drinking. Renin substrate, angiotensin I and angiotensin III produced greater intakes at forebrain tissue sites than after i.c.v. or subfornical organ injections. Renin, on the other hand, was more potent i.c.v. than at forebrain loci. These results suggest that the cerebral renin-angiotensin system may participate in beta-adrenergic thirst mechanisms by increasing local angiotensin II biosynthesis in specific areas of the brain.

Animals↗

PubMed1986

The role of the renin-angiotensin system in compound 48/80-induced thirst in rats.

The role of the renin-angiotensin system in compound 48/80 (3 mg/kg s.c.)-induced thirst in rats was investigated. Bilateral nephrectomy attenuated drinking induced by compound 48/80 but not by polyethylene glycol (PEG) (30%, 5 ml s.c.). Pretreatment with tripelennamine (histamine H1-receptor antagonist, 40 mg/kg i.p.) prior to the administration of compound 48/80 reduced the effect of compound 48/80 on drinking, but pretreatment with cimetidine (histamine H2-receptor antagonist, 40 mg/kg i.p.) or propranolol (beta-adrenoceptor antagonist, 10 mg/kg i.p.) had no effect. The effect of SQ 14,225 (angiotensin converting enzyme inhibitor) in various concentrations (0.5-100 mg/kg s.c.) was investigated on the drinking response caused by compound 48/80 (3 mg/kg s.c.), PEG (30%, 5 ml s.c.), isoprenaline (0.5 mg/kg s.c.) and hypertonic saline (5.8%, 2 ml s.c.). SQ 14,225 at a dose of 50 mg/kg significantly attenuated the compound 48/80-induced water intake when administered within 30 min prior to the injection of compound 48/80. Pretreatment with a high dose of SQ 14,225 (50 or 100 mg/kg s.c.) 15 min prior to the injection of dipsogens caused inhibition of the drinking response to compound 48/80 or isoprenaline, but not to PEG or hypertonic saline. Pretreatment with lower doses of SQ 14,225 (0.5 or 5 mg/kg, s.c.) had no inhibitory effect on compound 48/80- or isoprenaline-induced water intake. The inhibition of water intake by SQ 14,225 seems to be dependent on the dose and time between administration of SQ 14,225 and compound 48/80 or isoprenaline. Compound 48/80 and hypertonic saline were additively effective in producing the drinking response.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1982

Opiate receptor blockade in man reduces 2-deoxy-D-glucose-induced food intake but not hunger, thirst, and hypothermia.

Opioid peptides may act as neuromodulators in the central nervous system to conserve energy stores and water in mammals. To examine this hypothesis in man, the effect of opiate receptor blockade with naloxone on the hunger, thirst, and hypothermic response to 2-deoxy-D-glucose-induced glucoprivic stress was assessed. Opiate receptor blockade decreased stress-induced food intake but did not reduce marked increases in hunger produced by glucoprivation. Naloxone infusions did not change the hypercortisolemic, polydipsic, hypothermic, and thermogenic response to 2-deoxy-D-glucose. While these results do not suggest a major role for a beta-endorphin modulation of stress-induced hunger, hypothermia and water conservation, the reduction of food intake could be due to augmented satiety, perhaps associated with retardation of gastric emptying during opiate receptor blockade.

Blood Glucose↗

PubMed1975

Graded levels of hemorrhage, thirst and angiotensin II in the rat.

Hemorrhage was evaluated as a stimulus to drink in rats prepared with chronically implanted jugular cannulae and bled either 20, 30, 40 or 50 percent of their total blood volume. Hourly observations of water intake for 5 hr after hemorrhage revealed that the volume drunk was proportional to the degree of hemorrhage. Drinking induced by 20 percent hemorrhage did not differ significantly from control values, and intake was greatest and most persistent after 50 percent blood loss. The onset of maximal drinking at 1 hr after 40 percent hemorrhage was preceded by a twofold increase in plasma concentrations of angiotensin II. This is compatible with previous suggestions that angiotensin plays a role in hypovolemic thirst.

Angiotensin II↗

PubMed1984

The subfornical organ and the integration of multiple factors in thirst.

Rats with lesions centered on the ventral stalk of the subfornical organ (SFO) were used to characterize the participation of this structure in the control of drinking. It is concluded that the SFO does indeed play some minor role in the mediation of drinking following intraventricular injections of angiotensin. Further, it is shown that lesions of the SFO, but not lesions of the adjacent septal-hippocampal tissue, attenuate osmotic thirst elicited by two doses of hypertonic saline. Diminished drinking responses following water deprivation, and normal feeding responses following food deprivation, underscore the importance of the SFO for drinking behavior in general, and an expanded role for the SFO in fluid regulation is suggested. However, some incidental observations suggest that the SFO is less than an equal partner with structures in the AV3V region in the overall control of water balance.

Angiotensin II↗

PubMed1990

Thirst and sodium appetite in Dahl rats.

In confirmation of a previous study, rats of the Dahl S and R sublines exhibited no spontaneous preference for dilute NaCl solutions and an aversion for isotonic and hypertonic NaCl solutions when they were offered in a 2-bottle choice with water. A hysteresis effect was observed when choice was offered between water and a descending series of concentrations of NaCl solution compared with a preceding increasing series. In response to either chronic dietary administration of an angiotensin I converting enzyme inhibitor (ACEI) or acute sodium depletion, rats of the R subline developed a strong NaCl appetite, but the S subline did not. In contrast, rats of both sublines showed an NaCl appetite in response to a regimen of deoxycorticosterone acetate (DOCA). In acute drinking tests, rats of the S subline drank less water than those of the R subline in response to administration of either isoproterenol, ACEIs, or hypovolemia. Both R and S sublines drank similar amounts of water after SC administration of angiotensins I and II, and hypertonic NaCl. Compared with R rats, S rats had lower plasma renin activity in several of the above conditions, and their decreased thirst and sodium appetite appears to be a direct result of an underactive renin-angiotensin system.

Animals↗