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Thirst following water deprivation in dogs.

Eight dogs were prepared with unilateral carotid loops, and trained to stand quietly in a modified Pavlov stand. They were deprived of water for 24 h, which significantly depleted both the cellular and extracellular fluid (ECF) compartments. When they were allowed access to water for 5 min, they promptly drank amounts sufficient to make up their fluid deficits. Infusion of water into the unilateral carotid loop to reduce the cerebral blood osmolality to normal did not consistently reduce drinking because of inadequate mixing in the Circle of Willis. The eight dogs were then prepared with bilateral loops and deprived of water. Infusion of water at 0.6 ml-kg-1-,min-1 reduced the jugular plasma osmolality to control levels but did not affect systemic osmolality and reduced the drinking by 72%. Intracarotid infusion of water at differing rates reduced drinking in a dose related fashion. Intravenous infusion of 0.15 M NaCl in an amount designed to expand the ECF volume to normal reduced drinking by 27%. Expansion of the ECF volume plus bilateral intracarotid infusion of water to remove the central osmotic stimulus completely inhibited drinking. It is concluded that drinking following water deprivation in dogs is controlled by both central osmotic and by extracellular fluid volume factors, and that the osmotic factor is the more important. The drinking stopped well before these fluid deficits, as judged by body fluid analysis, had been restored. Some other mechanisms, therefore, must be involved in satiety.

Animals

Blood changes in water deprived rats.

To study the variations of blood constituents during water deprivation, rats were deprived of water from six to twelve days. Control and rehydrated animals were also included in the study. A significant increase was observed in sodium, chloride and hematocrit throughout the experiment. Calcium, bicarbonate and PCO2 increased at 10-11 days of treatment. Potassium, inorganic phosphorus, pH, base excess and blood buffer capacity did not change in the course of the experiment. Rehydrated animals recovered to control levels in all the studied components, except for pH and base excess, which increased somewhat. Plasma volume changes could explain only partially electrolyte variation. The "dehydration reaction" is considered to be the main mechanism responsible for these changes. Unchanged hematocrit levels in water deprived animals suggest that after 6 days of water deprivation there is no further loss of plasma water. Bicarbonate and PCO2 changes showed a good relationship and may account for unchanged pH and base excess values.

Acid-Base Equilibrium

Inhibition of thermal tachypnoea in rabbits following exposure to cold and water deprivation.

1. Rabbits were clipped and exposed in turn to four environmental conditions: control (C), cold exposure (CE), water deprivation (WD) and water deprivation and cold exposure together (WD/CE). 2. Following each type of treatment, the rabbits were exposed for 1 hr to an ambient temperature (Ta) of 35 degrees C. During this time, respiratory frequency (RF), rectal temperature (Tre), activity and oxygen consumption (V02) were recorded. 3. It was found that under both cold exposure and water deprivation conditions, the mean respiratory frequency during the first 30 min of heat exposure was reduced when compared with controls. This was associated with a delay in the onset of thermal tachypnoea. Under conditions of water deprivation and cold exposure together, the mean respiratory frequency was further reduced and the length of the delay was increased. 4. Previous cold exposure led to an increase in the V02 measured at 35 degrees C, whereas the V02, after water deprivation and water deprivation and cold exposure together were not significantly different from the control. 5. Neither the initial Tre nor the change in the Tre during the course of the heat exposure were significantly different from the controls under any of the experimental conditions. 6. It is concluded that both water deprivation and previous cold exposure cause a block to panting in the heat and that the blocking mechanisms involved are closely interrelated. It is also concluded that neither the metabolic rate of the animal nor its initial or final Tre are important factors in determing the degree to which thermal tachypnoea is inhibited.

Animals

Body fluid changes which influence drinking in the water deprived rat.

1. After overnight deprivation of water both the cellular and extracellular fluid volumes are significantly reduced in the rat. 2. In the rat with functional kidneys oral, intragastric or intravenous preloads of 10 ml. water reduce the total water intake after 1 hr by 64-69%. These preloads restore plasma osmolality to pre-deprivation levels but have little effect on plasma volume. 3. In the same rats if the plasma volume is restored with an oral, intragastric or intravenous preload of 10 ml. of an isotonic balanced salt solution which has little effect on osmolality, drinking is significantly reduced by 20-26%. The reduction of drinking correlated with the volume of the preload of balanced salt. 4. Plasma analysis shown that 1 hr after an oral preload of 10 ml. isotonic balanced salt solution, the extracellular fluid volume of the deprived rats is restored to pre-deprivation levels but osmolality is unchanged. Three hr after the balanced salt preload, extracellular fluid volume is still at pre-deprivation levels and there has been a slight decrease in osmolality due to excretion of salt. 5. In rats which had been nephrectomized or had the ureters ligated so there could be no renal modification of the preloads, the effects of the preloads of water and balanced salt are the same as in rats with intact kidneys. 6. The results indicate that after water deprivation in the rat, changes in both the cellular and extracellular fluid compartment are stimuli to drinking.

Animals

Mechanism of the decreased erythropoiesis in the water deprived rat.

Radioiron uptake by erythrocytes, metabolic rate, erythropoietin formation during hypoxia and erythroid responsiveness to exogenous erythropoietin were determined in both starved and water deprived rats. The feed intake showed a marked and progressive reduction during water deprivation. The metabolic rates of rats deprived of either food of water declined progressively showing a 40% reduction 5d after water deprivation or starvation began. At this time, the 24 h red blood cells 59Fe incorporation was 85% lower in both starved and dehydrated rats than in normal rats. Plasma erythropoietin levels in response to hypoxia were approximately 50% decreased in both starved and dehydrated rats. Both polycythaemic starved and polycythaemic water deprived rats injected with human urinary erythropoietin showed a 75% decrease in 59Fe incorporation into erythrocytes when compared to control rats. It is suggested that depression of erythropoiesis during water deprivation in the rat depends on a reduced sensitivity to erythropoietin, possibly associated with decreased production of the hormone. Since water deprived rats drastically reduce feed intake it is suggested that secondary starvation is the principal cause of the decreased erythropoiesis induced in the rat by water deprivation.

Animals

Effect of rehydration of rat liver tissue after water deprivation.

Male albino rats were deprived of water for 6 days, then they were allowed to drink tap water ad libitim. The structure of the liver was examined by light and electron microscopy, and the protein and dry matter contents, oxygen consumption and glucose-6-phosphatase activity of the liver were determined after rehydration. At 10 minutes, the mitochondria showed signs of division and a peculiar transformation of the cristae. At 60 minutes, the membranes of the rough endoplasmic reticulum were found to have proliferated. At 12 hours, the smooth-surfaced membranes showed hypertrophy and the bile canaliculi were distended. At 24 hours all rehydration induced organelle alterations were declining. The biochemical findings agreed well with the fine structural changes and both were indicative of an enchanced functional capacity of liver cells during rehydration.

Animals

The effect of water deprivation on lithium clearance and lithium excretion fraction in lithium-polyuric rats.

The effect of water deprivation on lithium clearance was studied in rats with lithium-induced polyuria. During a 3-hr period of water deprivation, the rats lost water in amounts corresponding to about 10% of body weight. Lithium clearance fell to about 25% of the level observed in rats which were not water deprived. During shorter periods of water deprivation, the fall of lithium clearance was less. The decrease of lithium clearance was partly due to a fall of inulin clearance and partly due to a fall of fractional excretion of lithium. The decrease of the two variables contributed to the same extent to the decrease of lithium clearance. The findings support the suggestion that insufficient intake of water in patients with lithium-induced polyuria may lead to a rapid lowering of lithium clearance and, hence, to a rise of the serum lithium concentration and development of intoxication.

Animals

Changes of plasma volume and plasma composition in water-deprived rats.

Plasma volume, hematocrit, protein and electrolyte concentrations in plasma were measured in control and water-deprived rats every three days after starting the experiment until the 15th day. Plasma volume variations, as related to body weight, suggest that water loss from plasma was proportional to total body water at three days and after 9 days of water deprivation. Greater plasma water than body water loss was found during the period between 3 and 9 days. Plasma protein and electrolyte variations suggest that during water deprivation there is a loss of protein, sodium and potassium from plasma, which is proportionally less than that of plasma water. Potassium, calcium and inorganic phosphorus were lost proportionally to plasma water. The variations in plasma volume changes were partially explained as due to variations in plasma protein and electrolyte concentrations.

Animals

Evaluation of a modified water-deprivation test for diagnosis of polyuric disorders in dogs.

A modified water-deprivation test was performed on 12 polyuric and 4 clinically normal dogs. Immediately after maximal urine osmolality had been achieved with water deprivation, antidiuretic hormone was injected to test further renal concentrating ability. The test provided accurate diagnosis of severe hypothalamic-neurohypophyseal diabetes insipidus in 3 dogs, partial diabetes insipidus in 2 dogs, and primary (psychogenic) polydipsia in 2 dogs. Five polyuric dogs with hyperadreno corticism had a response to the modified water-deprivation test similar to that of dogs with partial diabetes indipidus.

Adrenocortical Hyperfunction

Inhibition of drinking in water-deprived rats by combined central angiotensin II and cholinergic receptor blockade.

The effect of blockade of central angiotensin II (AII) receptors and cholinergic receptors on thirst induced by water deprivation was studied in Sprague-Dawley rats and rats with hereditary hypothalamic diabetes insipidus (DI). Neither central AII nor cholinergic blockade alone affected drinking. Antagonism of both receptors simultaneously, however, significantly inhibited water intake of both Sprague-Dawley and DI rats. This inhibitory effect was not observed in water-deprived, nephrectomized rats. The combined antagonism on water intake was specific, since milk intake in hungry rats was not affected by simultaneous AII and cholinergic blockade. Isorenin concentrations in brain tissue were at control levels in water-deprived, nephrectomized, and non-nephrectomized Sprague-Dawley rats but were increased in water-deprived DI rats. The results suggest that angiotensin and cholinergic receptors in the brain have a physiological role in thirst. Thirst is maintained when either receptor is intact, but reduced when both receptors are inhibited by antagonists. They are independently capable of maintaining thirst.

Animals

Water-intake volume regulation in the rat: schedule-induced drinking compared with water-deprivation-induced drinking.

Hungry rats drink extremely large amounts of water when they are intermittently fed small amount of food (schedule-induced polydipsia). Are such animals motivated to drink for long durations, to ingest large amounts of fluid, or to do both? When drinking-tube apertures were decreased to slow the rate of water ingestion, each of eight rats spent more time drinking (M = 11.5 min) than when larger apertures were used (M = 7.8 min). The mean volumes ingested were not different. These equal volumes were generated by adjustment of each drink duration in accordance with ingestion rate even during the first few drinks of the sessioons, even when the drinking tubes were frequently switched (every 1-3 min) during the sessions. During drinking induced by water deprivation when food was concurrently available, restriction of the driking-tube apertures reduced intake volumes by 18%-19%. However, when food was not concurrently available during water-deprivation-induced driking, regulation of intake volumes was comparable with that found during schedule-induced polydipsia. These data pose difficulties for theories that ascribe a crucial role to the motor aspects of schedule-induced drinking.

Animals

Hypothalamic supraoptic neurones: rates and patterns of action potential firing during water deprivation in the unanaesthetized monkey.

Extracellularly recorded action potentials were obtained from hypothalamic supraoptic neurones in unanaesthetized rhesus monkeys. Rates and patterns of firing were studied during an initial control period, during 5 successive days of water deprivation and during 4 further days when drinking water was again available. During water deprivation, plasma osmolarity increased progressively from about 300 mOsmoles/kg to about 340 mOsmoles/kg; control values were again reached after 3 days of rehydration. Systematic changes in action potential firing accompanied the changes in plasma osmolarity. Under control conditions, the majority of cells fire slowly and irregularly (type i), whilst a few cells exhibited phases of alternating activity and silence (type p). As dehydration progresses, the frequency of neuronal firing increase and the pattern of firing changes. By the third day the majority of cells are type p with few type i cells being found. By the fourth day, the population consists of type p cells with some others showing a high continuous rate of firing (type c). By the fifth day, these two cell types are found in approximately equal proportions. Rehydration of the animal reverses the situation. We propose that type i cells contribute little, if at all, to hormone secretion, while type p and type c cells would be in a more actively secreting state. According to this view, the three firing patterns would represent different activity states of the same functional population stimulated by the unspecific stimulus of water deprivation rather than functionally different neurones. However, the use of stimuli which selectively release either oxytocin or vasopressin may be needed to answer this problem.

Action Potentials

Substance P-like content in the hypothalamus of water-deprived rats.

The content of substance P-like in the hypothalamus of control and dehydrated rats was determined by bioassay on isolated jejunum of rabbits. Depriving the rats of drinking water for twelve days caused statistically significant increase of the substance P-like in the hypothalamus. These results suggest that water deprivation increases the synthesis of substance P-like in the rat hypothalamus.

Animals

Interresponse time changes as a function of water deprivation and amphetamine.

Drug effects on operant behavior are often characterized by their effects on rate of responding, usually expressed as the number of responses per unit of time. The time between two consecutive responses constitutes an interresponse time (IRT), and this measure has been used also to characterize the effects of drugs on operant behavior. IRTs which occur during a session can be classified on a statistical basis as: 1) short-IRT, an IRT(s) of short duratio generated by high-frequency responses; 2) pause, an IRT of long duratio generated by low-frequency responses; and 3) post-reinforcement pause, an IRT which immediately follows reinforcement. This investigation used three schedules of water reinforcement (fixed-ratio 20, fixed-interval 90-seconds and variable-interval 20-seconds) to examine how these IRT classes are influenced by changes in water deprivation conditions or amphetamine administration. Base-line IRT distributions depended upon the schedule of reinforcement. Changes induced by doses of amphetamine or alterations in level of water deprivation were compared and contrasted. Short-IRTs that characterized fixed-ratio 20 performance were resistant to change with increasing doses of amphetamine, but were increased in duration with decreasing water deprivation. Animals responding on a fixed-interval 90-second schedule showed a decreased postreinforcement pause after amphetamine, but an increased postreinforcement pause after access to water. An additional experiment studied the combined effects of presession water consumption and d-amphetamine administration on variable interval performances. Making water available before the session lowered the amphetamine dose-response curve along the vertical axis, suggesting that amphetamine did not mimic satiation. In most cases the effect of amphetamine and changing levels of water deprivation were dissimilar in their effects on IRT distributions, suggesting that amphetamine does not exert its major action on behavior through its adipsic effect.

Amphetamine

The effect of food and water deprivation and satiation on recognition.

Food and water deprived and satiated subjects, as well as control subjects, were shown words presented tachistoscopically for .01 sec until word recognition. Five food-relevant, five water-relevant, and five neutral (animal) words of high string frequency were matched for letter confusability and letter predictability. Analyses of the data, in terms of number of presentations until recognition as well as number of words recognized at selected presentations, revealed that the amount but not the type of deprivation significantly altered word recognition. Moreover, the effect of motivation was significant already on the first slide presentation, while the effects of word characteristics (word category and generated value) occurred only after a number of presentations.

Drive

The effect of intraventricular 6-hydroxydopamine on the content of oxytocin and vasopressin in the hypothalamus and pituitary gland of water-deprived rats.

The effect of intraventricular 6-hydroxydopamine on the content of oxytocin and vasopressin in the hypothalamus and pituitary gland of water deprived rats. Acta Physiol. Pol., 1977, 28 (6): 497-504. Rats received one infusion of 200 microgram 6-hydroxydopamine with 25 microgram of ascorbic acid into the lateral cerebral ventricle. After 57 days some rats were deprived of water for 4, 8 or 12 days. Then, the animals were sacrificed by decapitation. Oxytocin was determined in extracts from the posterior pituitary lobe and hypothalamus by the method of Van Dongen and Hays, while the vasopressin content was determined by the method of Dekanski. It was found that 6-hydroxydopamine injection into the cerebral ventricles causes a rise in oxytocin content in the hypothalamus and prevents its fall during--4--12 days of dehydration.

Animals

Drinking behavior in water deprived rats after angiotensin receptor blockade.

Angiotensin II is a peptide normally present in the bloodstream and central nervous system. Exogenous angiotensin induces drinking which is inhibited by saralasin, a specific receptor antagonist. Administration of saralasin does not reduce endogenously stimulated drinking. Angiotensin is dipsogenic after intravenous or intracerebroventricular infusion, raising the possibility of multiple access routes to the brain. Water deprived rats were given saralasin by both routes simultaneously to block the access of endogenous angiotensin to recentors reached from blood and ventricular cerebrospinal fluid (CSF). Water deprivation increased plasma (Na+), hematocrit, vasopressin content and renin activity but saralasin treatment did not reduce water intake after 30 or 60 min. Therefore, blood or CSF-bore angiotensin does not appear to be an absolute requirement for water deprivation drinking behavior.

Angiotensin II

Acid phosphatase in rat neurohypophyseal dispersions and its fractions enriched for neurosecretosomes and pituicytes after water deprivation and lactation.

Neurohypophyseal dispersions and fractions enriched for neurosecretosomes and pituicytes were prepared from rats subjected to 6 days of water deprivation and 9-10 days of lactation as stimuli of the hypothalamo-neurohypophyseal system (HNS). After water deprivation the content of the fractions changed in such a way that the neurosecretosomes, and to a lesser extent also the pituicytes, accumulated at a lower density within the gradient used for separation. Stimulation by means of lactation did not show such changes when a comparison was made with dioestrus. Microchemical and histochemical tests for acid phosphatase showed that most of the activity in the controls was present in the neurosecretosomes. A rough calculation, which takes into account the different yields for the dispersion elements, showed a rather equal distribution for acid phosphatase activity between axonal and pituicytic compartments of the intact neurohypophysis. The known acid phosphatase activity response of the neural lobe after HNS stimulation, which was also detectable in the dispersion, resulted histochemically in an increased staining intensity for both neurosecretosomes and pituicytes, but with microassay it was distributed along a gradient similar to oxytocin. It was therefore concluded that this lysosomal enzyme response within the neurophypophysis is preferentially localized in the neurohypophysis is preferentially localized in the neurosecretory axons.

Acid Phosphatase