Thirst and salt appetite responses in young and old Brown Norway rats

Male Brown Norway rats aged 4 mo (young) and 20 mo (old) received a series of experimental challenges to body fluid homeostasis over approximately 3 mo. Water was available for drinking in some tests, and both water and 0.3 M NaCl were available in others. The series included three episodes of extracellular fluid depletion (i.e., furosemide + 20 h of sodium restriction), two tests involving intracellular fluid depletion (i.e., hypertonic saline: 1 or 2 M NaCl at 2 ml/kg body wt sc), one test involving overnight food and fluid restriction, and testing with captopril adulteration of the drinking water (0.1 mg/ml) for several days. Old rats were significantly heavier than young rats throughout testing. Old rats drank less water and 0.3 M NaCl after sodium deprivation than young rats, in terms of absolute and body weight-adjusted intakes. Old rats drank only half as much water as young rats in response to subcutaneous hypertonic NaCl when intakes were adjusted for body weight. Old rats drank less 0.3 M NaCl than young rats after overnight food and fluid restriction when intakes were adjusted for body weight. In response to captopril adulteration of the drinking water, young rats significantly increased daily ingestion of 0.3 M NaCl when it was available as an alternative to water and significantly increased daily water intakes when only water was available, in terms of absolute and body weight-adjusted intakes. Old rats had no response to captopril treatment. These results add important new information to previous reports that aging rats have diminished thirst and near-absent salt appetite responses to regulatory challenges.     

Gestational and early postnatal dietary NaCl levels affect NaCl intake, but not stimulated water intake, by adult rats

We examined body fluid regulation by weanling (21-25 days) and adult (>60 days) male rats that were offspring of dams fed chow containing either 0.1, 1, or 3% NaCl throughout gestation and lactation. Weanling rats were maintained on the test diets until postnatal day 30 and on standard 1% NaCl chow thereafter. Ad libitum water intake by weanlings was highest in those fed 3% NaCl and lowest in those fed 0.1% NaCl. Adult rats maintained on standard NaCl chow consumed similar amounts of water after overnight water deprivation or intravenous hypertonic NaCl (HS) infusion regardless of early NaCl condition. Moreover, baseline and HS-stimulated plasma Na(+) concentrations also were similar for the three groups. Nonetheless, adult rats in the early 3% NaCl group consumed more of 0.5 M NaCl after 10 days of dietary Na(+) deprivation than did rats in either the 1% or 0.1% NaCl group. Interestingly, whether NaCl was consumed in a concentrated solution in short-term, two-bottle tests after dietary Na(+) deprivation or in chow during ad libitum feeding, adult rats in the 3% NaCl group drank less water for each unit of NaCl consumed, whereas rats in the 0.1% NaCl group drank more water for each unit of NaCl consumed. Thus gestational and early postnatal dietary NaCl levels do not affect stimulated water intake or long-term body fluid regulation. Together with our previous studies, these results suggest that persistent changes in NaCl intake and in water intake associated with NaCl ingestion reflect short-term behavioral effects that may be attributable to differences in NaCl taste processing.     

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.     

Water ingestion provides an early signal inhibiting osmotically stimulated vasopressin secretion in rats

Dehydrated dogs are known to inhibit secretion of vasopressin (VP) within minutes after drinking water, before plasma osmolality (P(osmol)) diminishes. The present studies determined whether water ingestion causes a similar rapid inhibition of neurohypophyseal hormone secretion in rats. Adult rats were infused with 1 M NaCl (2 ml/h iv) for 240 min to stimulate VP and oxytocin (OT) secretion. After 220 min of infusion, rats were given water to drink for 5 min, and blood samples were taken 5 and 15 min later for RIA. Plasma VP (pVP) was much lower when rats ingested water than when they drank nothing even though P(osmol) was not significantly altered. Plasma OT (pOT) was affected similarly. In contrast, no effects on pVP or pOT occurred when rats drank isotonic NaCl solution for 5 min in amounts comparable to the water intakes (approximately 5.5 ml). These results suggest that neurohypophyseal secretion of VP and OT in rats is inhibited rapidly by water drinking, and that this inhibition is mediated by a visceral signal of osmotic dilution rather than by the act of drinking per se.     

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.     

Mice lacking the transient receptor vanilloid potential 1 channel display normal thirst responses and central Fos activation to hypernatremia

Neurons of the organum vasculosum of the lamina terminalis (OVLT) are necessary for thirst and vasopressin secretion during hypersmolality in rodents. Recent evidence suggests the osmosensitivity of these neurons is mediated by a gene product encoding the transient receptor potential vanilloid-1 (TRPV1) channel. The purpose of the present study was to determine whether mice lacking the TRPV1 channel had blunted thirst responses and central Fos activation to acute and chronic hyperosmotic stimuli. Surprisingly, TRPV1-/- vs. wild-type mice ingested similar amounts of water after injection (0.5 ml sc) of 0.5 M NaCl and 1.0 M NaCl. Chronic increases in plasma osmolality produced by overnight water deprivation or sole access to a 2% NaCl solution for 48 h produced similar increases in water intake between wild-type and TRPV1-/- mice. There were no differences in cumulative water intakes in response to hypovolemia or isoproterenol. In addition, the number of Fos-positive cells along the lamina terminalis, including the OVLT, as well as the supraoptic nucleus and hypothalamic paraventricular nucleus, was similar between wild-type and TRPV1-/- mice after both acute and chronic osmotic stimulation. These findings indicate that TRPV1 channels are not necessary for osmotically driven thirst or central Fos activation, and thereby suggest that TRPV1 channels are not the primary ion channels that permit the brain to detect changes in plasma sodium concentration or osmolality.     

Plasma Osmolality Predicts Extracellular Fluid Catechol Concentrations in the Lateral Hypothalamus

The lateral hypothalamus has an important role in regulating food and water intake. We have investigated the endogenous release of monoamines from the lateral hypothalamus during manipulations of plasma osmolality and circulating volume. Adult male Sprague-Dawley rats implanted with carbon paste in vivo electrochemical (EC) electrodes in the lateral hypothalamus were placed on a 72-h water deprivation schedule. Although the carbon paste EC electrode has an intrinsically ambiguous signal in which changes in ascorbic acid may appear as changes in catechol concentrations, pharmacologic studies in lateral hypothalamus indicated that the electrode most likely measured norepinephrine and possibly epinephrine. On the test day, the EC electrodes were scanned with linear sweep voltammetry from -0.2 to +0.4 V at a rate of 5 mV/s. Semiderivative signal processing showed catechol and hydroxyindole peaks at +0.11 and +0.23 V, respectively. Baseline recordings were made prior to rats drinking distilled water, 10% sucrose, 5% dextrose, 0.30% NaCl, 0.90% NaCl, or 10% d-mannitol. To control for the act of drinking, other implanted dehydrated rats were intraperitoneally injected with 5% dextrose, 0.30% NaCl, or 0.90% NaCl. To dissociate the effects of osmolality and circulating volume on the EC response, hydrated rats implanted with EC electrodes were subcutaneously injected with 12% NaCl or intraperitoneally injected with 35% polyethylene glycol. Other rats subjected to water deprivation and osmotic challenges were decapitated and trunk blood was collected for measurements of plasma osmolality and hematocrit. Similar experiments were conducted using homozygous Brattleboro rats which lack arginine vasopressin (AVP) but which preserve normal plasma osmolality with prodigious drinking.(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of the subfornical organ on meal-associated drinking in rats

A lesion of the subfornical organ (SFO) may disrupt drinking after a meal of dry chow as it does drinking after intragastric administration of hypertonic saline. Food and water intakes of SFO-lesioned (SFOX) and sham-lesioned rats were measured during 90-min tests following various lengths of food deprivation. During the tests, all rats began eating before they began drinking. After 20-24 h of food deprivation, latency to begin drinking after eating had started was longer for SFOX than for sham-lesioned rats. Plasma osmolality was elevated by 2-3% in both lesion groups at 12 min, the latency for sham-lesioned rats to drink, but SFOX rats nevertheless continued eating and delayed drinking. Eating after shorter 4-h food deprivations and ad libitum feeding produced more variable drinking latencies and less consistent effects of SFO lesion. During 24 h of water deprivation, SFO lesion had no effect on the suppression of food intake and did not affect food or water intakes during the first 2 h of subsequent rehydration. These findings indicate that the SFO is involved in initiating water intake during eating and in determining drinking patterns and the amount of water ingested during a meal.     

Amiloride-sensitive signals and NaCl preference and appetite: a lick-rate analysis

Rats prefer hypotonic and isotonic NaCl solutions to water in long-access drinking paradigms. To focus on the role of taste signals in NaCl preference, licking patterns of rats with 30-s exposure to NaCl solutions (0-0.5 M) were examined when they were either water deprived, sodium depleted, or not deprived (NaCl mixed in dilute sucrose). In all three conditions, rats displayed a preference for NaCl. The addition of 100 microM amiloride, a sodium channel blocker, to NaCl did not change rats' licking when they were sodium replete but dramatically reduced licking when they were deplete. Transection of the chorda tympani (CT) nerve, an afferent pathway for amiloride-sensitive Na(+) signals, had no effect on NaCl preference in nondeprived rats and only a modest effect on those that were Na(+) deplete. Amiloride was found to exert significant suppression of NaCl intake in Na(+)-depleted rats with transection of the CT, supporting the existence of other afferent pathways for transmission of amiloride-sensitive Na(+) signalling. Together, these studies argue for the involvement of different neural signalling mechanisms in NaCl preference in the presence and absence of explicit Na(+) need.     

Circulating angiotensin II mediates sodium appetite in adrenalectomized rats

We investigated the role of circulating ANG II in sodium appetite after adrenalectomy. Adrenalectomized rats deprived of their main access to sodium (0.3 M NaCl) for 9 h drank 14.1 +/- 1.5 ml of the concentrated saline solution in 2 h of access. Intravenous infusion of captopril (2.5 mg/h) during the last 5 h of sodium restriction reduced sodium intake by 77 +/- 12% (n = 5) without affecting the degree of sodium depletion and hypovolemia incurred during deprivation. Functional evidence indicates that this dose of captopril blocked production of ANG II in the peripheral circulation, but not in the brain; that is, injection of ANG I into the lateral brain ventricle stimulated intake of both water and 0.3 M NaCl. Intravenous infusion of ANG II (starting 10-15 min before 0.3 M NaCl became available) in adrenalectomized, captopril-treated rats restored both sodium intake and blood pressure to values seen in rats not treated with captopril. Longer (20 h) infusions of captopril in 22-h sodium-restricted rats also blocked sodium appetite, but reduced or prevented sodium depletion. Intravenous infusion of ANG II after these long captopril infusions stimulated sodium intake, but intake was less than in controls not treated with captopril. These results indicate that most or all of the sodium appetite of adrenalectomized rats is mediated by circulating ANG II.     

Central angiotensin receptor blockade impairs thermolytic and dipsogenic responses to heat exposure in rats

The effect of central angiotensin AT(1) receptor blockade on thermoregulation and water intake after heat exposure was investigated. Rats were placed in a chamber heated to 39 +/- 1 degrees C for 60 min and then returned to their normal cage (at 22 degrees C), and water intake was measured for 120 min. Artificial cerebrospinal fluid (5 microl) was injected intracerebroventricularly 60 min before heat exposure in five control rats. Colonic temperature increased from 37.22 +/- 0.21 to 40.68 +/- 0.31 degrees C after 60 min. In six rats injected intracerebroventricularly with 10 microg of the AT(1) antagonist losartan, colonic temperature increased from 37.41 +/- 0.27 to 41.72 +/- 0.28 degrees C after 60 min. This increase was significantly greater than controls (P < 0.03). Losartan-treated rats drank 1.1 +/- 0.4 ml of water compared with 5.9 +/- 0.77 ml (P < 0.002) drank by control animals, despite a similar body weight loss in the two groups. Central losartan did not inhibit the drinking response to intracerebroventricular carbachol in heated rats, suggesting that losartan treatment did not nonspecifically depress behavior. We conclude that central angiotensinergic mechanisms have a role in both thermoregulatory cooling in response to heat exposure and also the ensuing water intake.     

Water ingestion by rats fed a high-salt diet may be mediated, in part, by visceral osmoreceptors

After surgical removal of all salivary secretions ("desalivation"), rats increase their consumption of water while eating dry laboratory chow. In the present experiments, desalivated rats drank even more water while they ate "powdered" high-salt food (i.e., <15-mg food particles). The Na+ concentration of systemic plasma in these animals was not elevated during or immediately after the meal, which suggests that cerebral osmoreceptors were not involved in mediating the increased water intake. A presystemic osmoregulatory signal likely stimulated thirst because the Na+ and water contents of the gastric chyme computed to a solution approximately 150 mM NaCl. In contrast, desalivated rats drank much smaller volumes of water while eating "pulverized" high-salt food (i.e., 60-140-mg food particles), and the fluid mixture in the gastric chyme computed to approximately 280 mM NaCl solution. These and other findings suggest that the NaCl ingested in the powdered high-salt diet was dissolved in the gastric fluid and that duodenal osmoreceptors (or Na+-receptors) detected when the concentration of fluid leaving the stomach was elevated after each feeding bout, and promptly stimulated thirst, whereupon rats drank water until the gastric fluid was diluted back to isotonicity. However, when rats ate the pulverized high-salt diet, much of the NaCl ingested may have been embedded in the gastric chyme and therefore was not accessible to visceral osmoreceptors once it emptied from the stomach. Consistent with that hypothesis, fluid intakes were increased considerably when desalivated rats drank 0.10 M NaCl instead of water while eating either powdered or pulverized high-salt food.     

The role of renal nerves in the response to dipsogenic stimuli in the rat.

The effect of bilateral renal denervation on water intake and urine volume during specific thirst challenges was studied in rats. Renal denervation attenuated significantly the drinking response elicited by the administration of 30% polyethylene glycol (PG, extracellular challenge) but had no effect on the drinking response after an intracellular challenge (2.5 M NaCl) or after a 24-h water deprivation period. Furthermore, during a PG challenge total water intake was the same in two groups of rats, one with denervated kidneys and the other with beta-adrenergic neural activity in efferent renal nerves eliminated by blocking agents. Urine volumes were not affected by PG administration or water deprivation in denervated rats but were increased significantly after administration of 2.5 M NaCl. These results indicate that renal nerves play an important role in the physiological processes controlling extracellular thirst, and suggest that this role may be related to the neural control of release of renin.     

Vasopressin and oxytocin release evoked by NaCl loads are selectively blunted by area postrema lesions

The present study investigated the effect of area postrema lesions (APX) on stimulated neurohypophysial secretion of vasopressin (VP) and oxytocin (OT) in conscious rats. Blunted increases in plasma levels of both pituitary hormones were observed when rats with APX were infused intravenously with 1 M NaCl solution (2 ml/h for 6 h). In contrast, plasma VP and OT increased normally in rats with APX when equivalent increases in plasma osmolality (but not plasma Na(+)) resulted from intravenous infusion of an equiosmotic solution of 1 M mannitol and 0.5 M NaCl. Furthermore, APX did not affect increases in plasma VP and OT stimulated by plasma volume deficits, nor did APX disrupt OT secretion stimulated by intravenous injection of cholecystokinin. These findings suggest that the area postrema plays an important role in mediating secretion of VP and OT in response to an NaCl load, but not in response to an equiosmotic load that does not cause substantial hypernatremia, and not in response to other stimuli of neurohypophysial hormone secretion. Together with previous reports, these results suggest that APX impairs Na(+) regulation in rats.     

Centrally administered vasopressin cross-sensitizes rats to amphetamine and drinking hypertonic NaCl

Prior sodium restriction cross-sensitizes rats to the psychomotor effects of amphetamines and vice versa. Repeated central injections of vasopressin (VP) induce a psychomotor sensitization similar to amphetamine sensitization and repeated sodium deficiency. Thus brain VP signaling may be a common mechanism involved in mediating these two motivational systems. In experiment 1, we tested the hypothesis that rats previously sensitized to central VP would show enhanced psychomotor responses to amphetamine. Rats were administered saline, VP (50 ng), or amphetamine (1 mg/kg or 3 mg/kg) on days 1 and 2, and given saline or amphetamine on day 3. Amphetamine produced psychomotor arousal in all groups. However, amphetamine on day 3 elicited a significantly greater psychomotor response in rats that had prior injections of amphetamine or VP than in rats previously treated with saline. In experiment 2, the hypothesis that prior experience with central VP would cross-sensitize rats to drinking hypertonic sodium (NaCl) solutions was tested. Rats were administered VP (50 ng) or saline for 3 days. On the fourth day, nondeprived rats were given access to 0.3 M NaCl and water for 1 h. Control and saline-treated rats only drank 1 ml of 0.3 M NaCl, but rats previously exposed to central VP drank significantly more hypertonic saline (4 ml). These results show that prior experience with central VP cross-sensitizes rats to the psychomotor stimulant effects of amphetamine and the ingestion of concentrated NaCl solutions. This pattern of cross-sensitization links central VP signaling, amphetamine, and sodium deficiency, and therefore it may play a role in the cross-sensitization between sodium appetite and amphetamines.     

Water intake induced by water deprivation in the quail,Coturnix coturnix japonica

Mechanisms inducing drinking after water deprivation, and mechanisms terminating drinking after rehydration, were investigated in the quail, Coturnix coturnix japonica. 1. Water intake was induced after 4 h of water deprivation, and the amount of water drunk increased in proportion to the period of water deprivation. Drinking occurred immediately after deprivation. Drinking occurred immediately after deprived birds were given access to water, and continued for periods proportional to the period of water deprivation. 2. Plasma angiotensin II concentration increased, as did plasma osmolality and Na+ concentration, and blood volume decreased after water deprivation. The increase in plasma angiotensin II concentration and decrease in blood volume occurred soon after the start of water deprivation, whereas plasma osmolality and Na+ concentration did not increase until at least 4 h after the start of water deprivation. 3. These results indicate that extracellular dehydration and angiotensin II are responsible for the significant drinking that follows 4 h of water deprivation, and that cellular dehydration is also involved in the stimulation of drinking that occurs after longer periods of water deprivation. 4. Plasma osmolality and Na+ concentration in birds deprived of water for 48 h quickly returned to normal levels after the birds were allowed access to water. Plasma angiotensin II levels and blood volume also approached the values measured prior to water deprivation. However, the rate and degree of restoration of normal values were reduced, and normal values were not restored even after 1.5 h or rehydration when drinking terminated.(ABSTRACT TRUNCATED AT 250 WORDS)     

Circadian rhythms of food and 1% NaCl intake, urine and electrolyte excretion, plasma renin activity and insulin concentration in adrenalectomized rats

The circadian rhythms of food and 1% NaCl intake, and urine, Na+, Cl- and K+ excretion were followed up in male Wistar rats before and one week after bilateral adrenalectomy at 4-hour intervals during two consecutive days. The circadian rhythms of plasma renin activity (PRA) and plasma immunoreactive insulin (IRI) were evaluated after decapitation of both intact and adrenalectomized rats at 08, 16 and 24 h. To all rats 1% NaCl was offered instead of drinking water. Adrenalectomy did not cause any significant phase shift in the cosine curves approximating the data collected at 4-hour intervals. The circadian rhythms showed the same relationships before and after the operation: the rhythms of food intake, K+ excretion and saline intake preceded significantly the rhythms of urine, Na+ and Cl- excretion. Adrenalectomy induced an increase in mean PRA and shifted its minimal value from 08 to 24 h. After the operation mean IRI decreased and the minimal value shifted from 16 to 24 h. It was concluded that adrenal glands do not play an important role in the synchronization of the circadian rhythms of food and 1% NaCl intake, urine and synchronization of the circadian rhythms of food and 1% NaCl intake, urine and electrolyte excretion with the illumination cycle, but play a relevant role in the synchronization of the circadian rhythms of PRA and IRI in the rat.     

Inhibition of NaCl appetite when DOCA-treated rats drink saline

Marked increases in the consumption of concentrated NaCl solution were elicited in rats by daily injection of the synthetic mineralocorticoid, deoxycorticosterone acetate (DOCA). DOCA-treated rats drank different volumes of NaCl solution depending on its concentration (between 0.15 M and 0.50 M), with less consumed (in milliliters) the more concentrated the fluid was. In consequence, total Na(+) intake (in milliequivalents) was roughly similar in all groups. Gastric emptying of Na(+) also diminished as the concentration of the ingested NaCl solution increased, and the delivery of Na(+) to the small intestine was remarkably similar in all groups. Cumulative volume of ingested fluid in the stomach and small intestine was very closely related to intake (in milliliters) of the concentrated NaCl solutions. Systemic plasma Na(+) levels did not increase until after rats stopped consuming concentrated NaCl solution, although they were elevated at the onset of water ingestion. The situation appeared to be different when 0.15 M NaCl was consumed. This isotonic solution emptied and was absorbed relatively rapidly, and DOCA-treated rats drank larger amounts of it throughout a 1-h test period than when they drank concentrated NaCl solutions. Collectively, these findings suggest that saline consumption by DOCA-treated rats may be inhibited by two presystemic factors, one related to the volume of ingested fluid (i.e., distension of the stomach and small intestine) and one related to its concentration (i.e., elevated osmolality of fluid in the small intestine and/or in adjacent visceral tissue).     

Effects of dehydration,rehydration, and hyperhydration in the lactating and non-lactating black Moroccan goat

The effects of water deprivation, rehydration and hyperhydration were investigated in the black Moroccan goat (Capra hircus). Mean daily water intake was 46 ± 5 ml/kg in lactating and 36 ± 4 ml/kg in non-lactating black Moroccan goats, and milk production 21 ± 1 ml/kg. Mean urine excretion was 8 ± 2 ml/kg body weight in both groups, and the daily water losses via evaporation and feces were estimated at 23 ± 3 ml/kg during lactation and 28 ± 4 ml/kg during non-lactation. Forty-eight hours of water deprivation caused a body weight loss of 9% and 6% in lactating and non-lactating goats, respectively, and a drop of 28% in milk production with only a slight decrease in food intake. After rehydration, the elevated plasma osmolality as well as Na and total protein concentrations returned to basal values within 2–3 hr, indicating a rapid absorption of the ingested water, but urine excretion did not increase. After hyperhydration (10% of body weight), 46% of the load was excreted by the kidneys within 6 hr. In conclusion, black Moroccan goats have a low water turnover, and they can retain water upon rehydration but not store excess water after hyperhydration.     

Water balance during saline imbibition in the Mongolian gerbil (Meriones unguiculatus)

1. There were few changes in the water balance of gerbils drinking 0.25 and 0.50 M NaCl solutions for 5 days. 2. Imbibition of 0.75 and 1.0 M saline resulted in some dehydration of the body fluids and considerable depletion of the neural lobe vasopressin store. 3. Although large amounts of NaCl were excreted, the maximum urine osmolality was considerably less than that found following water deprivation. 4. The imbibition of 1.0 M saline caused similar changes in water balance to water deprivation showing that little, if any, water was gained from this solution.