Thirst Responses Research Articles

Effects of ethanol ingestion on thirst and fluid consumption in humans.

To investigate the effects of ethanol on thirst, fluid intake was measured in 24 normal subjects for 3 h after consumption of 1.0 g/kg ethanol, with or without administration of a vasopressin analogue (DDAVP) before ethanol ingestion. Fluid consumption was reduced in subjects receiving DDAVP, suggesting that thirst after ethanol is largely secondary to dehydration due to inhibition of vasopressin release. Further, the effects of ethanol on salt-load-elicited thirst and fluid consumption in normal subjects were studied using intravenous hypertonic saline infusions. Subjects acted as their own controls and received 0.5 or 1.0 ml/kg ethanol 30 min before infusions on one day and an equal volume of fluid on another day. During infusions after ethanol, subjects experienced thirst later and at higher osmolalities. They also drank less immediately after infusions with prior ethanol ingestion. The relationship between thirst score and plasma osmolality was shifted to higher osmolalities by ethanol. Thus, although ethanol progressively causes thirst secondary to dehydration, it has a direct inhibitory effect on the thirst response to osmotic stimulation.

Chronic hyperprolactinemia reduces peripheral β-adrenergic responsiveness in male rats

The MtTW15 prolactin (PRL) secreting adenoma elevated serum PRL concentrations over controls within 5 weeks after tissue implantation. This treatment resulted in a significant reduction of peripheral β-adrenergic responsiveness as assessed by three different parameters. Isoproterenol-induced thrist was significantly attenuated in the MtTW15 rats. The decrease in the thirst response was proportional to the increase in serum PRL. Unanesthetized heart rates of both groups were not significantly different before isoproterenol was administered. However, following administration of the β-adrenergic agonist the heart rate response in rats with elevated PRL was significantly attenuated when compared to the controls. Elevation of serum PRL virtually abolished the elevation of tail skin temperature response associated with administration of isoproterenol. Collectively, these results suggest hyperprolactinemia reduces peripheral β-adrenergic responsiveness; however the mechanism for this reduced response remains to be elucidated.

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 β-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.

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.

Effects of specific dopamine lesions and dopamine receptor sensitivity on angiotensin II- and carbachol-induced thirst in rats.

A study was made of the effects of manipulating brain dopaminergic activity upon drinking induced by intracerebroventricular administration of angiotensin II or carbachol. Non-specific lesions induced by injecting 6-hydroxydopamine (6-OHDA) into the cerebroventricles caused a significant reduction in angiotensin-induced thirst without affecting carbachol drinking. specific 6-OHDA-induced lesions of the dopaminergic nigro-striatal pathway also attenuated the angiotensin-induced response, while unilateral lesions reduced and bilateral lesions almost completely abolished the effect. Again, the response to carbachol was unaffected. Chronic haloperidol treatment increased behavioural responses to the dopamine agonist apomorphine and significantly stimulated angiotensin-induced drinking without affecting response to carbachol. These studies provide support for the hypothesis that a dopaminergic event is involved in the angiotensin-induced thirst response and point to the need for a functioning dopaminergic nigro-striatal pathway for the full expression of this response.

Delayed drinking in response to electrical and thermal stimulation of the medial forebrain.

Water intake in response to electrical and thermal stimulation of the medial forebrain was studied in the goat. When the frontal wall of the third cerebral ventricle was included in a field of bipolar electrical stimulation a dipsogenic response was obtained after discontinuation of the stimulation. Release of antidiuretic hormone (ADH) was apparently also elicited. The water intake was roughtly proportional to the amount of current which had been applied during the stimulation period. Water consumption in response to stimulation attenuated the dipsogenic effect of subsequent stimulation, as did also pre-stimulatory hydration by stomach tube. A 2 degrees C elevation of the temperature of parts of the preoptic/anterior hypothalamic region for 40 min periods incuded cumulative drinking starting after 2.5 to 18 min. There were great interindividual differences in the amount of water consumed in response to the thermal stimulation, possibly due to variations in thermo-couple electrode placement. The dipsogenic effect of forebrain warming was inhibited by pre-hydration, and by lowering of the environmental temperature. The delayed thirst responses are discussed in relation to stimulus-bound drinking previously observed in the same and other species. It appears possible that the delayed drinking was a manifestation of artificially induced excitation of juxtaventricular "thirst" receptors.

Episodic secretion of arginine vasopressin.

The plasma arginine vasopressin (pAVP) response to osmotic stimulation was studied in dogs and sheep by sampling at frequent intervals during steady-state dehydration and during water diuresis. Frequent sampling also was conducted after continuous infusion or bolus injection of 5 or 20 g/100 ml NaCl. A pulsatile pattern of pAVP was observed after such infusions or injections and in some animals after water deprivation. This pattern was not seen after water loading or in mildly dehydrated animals. The short term changes in pAVP during continuous infusion of 5 g/100 ml NaCl could not be correlated with variations in plasma tonicity. Rather, they appeared to reflect discontinuous hypothalamic posterior pituitary release of AVP. Thirst was evoked by a lower dose of 5 g/100 ml NaCl than was required for consistent stimulation of pAVP release, and the thirst response frequently was observed prior to the peak AVP response after bolus injection of 5 and 20 g/100 ml NaCl.

ENDOGENOUS ANGIOTENSIN STIMULATION OF VASOPRESSIN (AVP) IN THE NEWBORN LAMB

Exogenous renin or anglotensin II (A II) infused peripherally or into the CNS will stimulate thirst and AVP release. Whether the endogenous renin-anglotensin system physiologically stimulates thirst or AVP secretion is unknown. To assess the effect of endogenous renin-angiotensin stimulation on AVP secretion in the lamb, nine normal newborn lambs were stimulated with furosemide (FU) 2 mg/kg infused I.V. alone, and with the A II inhibitor 1-sar, 8-ala, A II, 5 μg/kg/min. Six anephric lambs received only FU. Blood samples were drawn at 8, 20, 35, 65 and 125 min. post infusion. PRA (ng/ml/hr), aldosterone (aldo, ng/dl) and AVP (μU/ml) were measured by RIA. (M and SEM) PRA increased within 8 min. from a baseline of 16.7±5.0 to 30.2±12.3 (p<.05), and remained elevated through 120 min. Plasma Aldo and AVP increased post FU from respective baselines of 14.2±4.7 and 2.7±0.,5, to 28.5±13.2 and 9.9±3.5 at 35 min. (p<.05), and thirst-like behavior was observed. AVP, thirst, and Aldo did not increase after FU in anephric lambs or in normal lambs treated with A II inhibitor. There were no changes in mean plasma sodium, Hct, or osmolality, and minimal changes in systemic blood pressure and plasma protein concentration during the first 35 min, after FU. We conclude: 1) that FU stimulates Aldo, AVP and thirst via direct renal stimulation of renin, 2) the Aldo, AVP and thirst responses to FU are mediated by A II release and 3) these responses all are intact in the newborn period.

Persistent hypernatremia due to abnormal thirst mechanism in a 13-year-old child with nephrogenic diabetes insipidus

A 13-year-old mentally retarded boy with the clinical features of Prader-Willi syndrome and Pitressin-resistant polyuria was found to have persistent hypernatremia despite free access to water. His total body water, extracellular fluid, and plasma volume were reduced, and peripheral venous renin activity was increased. He drank 6 to 8 liters of fluid per 24 hours but still had a blunted thirst response as reflected by changes in serum sodium concentration, which varied as much as 12 mEq. per liter from morning to evening. His chronic hypernatremia is regarded as due to deranged thirst regulation and dehydration.

Observations on central control of drinking and of the release of antidiuretic hormone (ADH)

The thirst response to slow infusions of hypertonic NaCl into different parts of the 3rd brain ventricle of the goat was studied. The most efficient stimulation of the thirst mechanism was obtained by infusions into the anterior ventral part of the ventricle. Repeated brief infusions of hypertonic NaCl into this part of the 3rd ventricle gave a very consistent antidiuretic response in hydrated goats. Direct evidence that this antidiuresis was due to a release of endogenous ADH was obtained by the observation that the response disappeared when experimental diabetes insipidus had been produced.

A study of thirst and other effects of an increased sodium concentration in the 3rd brain ventricle.

ABSTRACTThe characteristics of thirst elicited by injections of hypertonic NaC1‐solution into the 3rd brain ventricle were studied in goats supplied with permanent ventricular canola. Animals in normal water balance drank 1.5 to 2.0 1 of water within 2 min after the intraventricular injection of 0.1 ml of 0.85 M NaC1. In the hydrated animal this thirst response was markedly diminished or completely absent. If the goats were not allowed to quench their thirst immediately after the intraventricular injection of hypertonic NaC1, the urge to drink gradually became weaker and disappeared after about 20 min. Single or repetitive injections of 0.1 ml of 0.85 M NaCl into the 3rd brain ventricle were further found to cause a conspicuous increasz in urinary excretion of Na+ and C1– and to inhibit temporarily an established water diuresis. Aldosterone treatment did not prevent the increase in urinary electrolyte excretion occurrinz after injections of hypertonic NaCl into the 3rd ventricle.Repetitive injections of 0.1 ml of 0.85 M NH4Cl or of 1.7 M d‐glucose into the 3rd ventricle, or injections of 0.1 ml of 0.85 M NaCl into the lateral ventricle did not induce drinking or cause any increase in urinary electrolyte excretion.