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Neurohypophyseal Hormones: From Genomics and Physiology to Disease
1Department of Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania; and 2Department of Psychology, Florida State University, Tallahassee, Florida
Submitted 7 October 2005 ; accepted in final form 22 November 2005
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ABSTRACT |
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 TOP ABSTRACT METHODSRESULTSDISCUSSIONREFERENCES |
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dehydration; gastrointestinal distension; visceral osmoreceptors; water deprivation
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METHODS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONREFERENCES |
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Adult male Sprague-Dawley rats (300–370 g; Harlan Laboratories) were housed singly in cages in the Biomedical Research Facility at Florida State University (experiment 1A) or in the Department of Neuroscience at the University of Pittsburgh (experiments 1B, 2A, and 2B). Both colony rooms were maintained at a constant temperature (22–23°C) and with a fixed light-dark cycle (lights off from 7:00 PM to 7:00 AM). All rats had >1 wk of ad libitum access to pelleted laboratory chow (5001, Purina) and tap water before experiments began.
Experimental Protocols
Experimental protocols were reviewed and approved by the Institutional Animal Care and Use Committees of Florida State University and of the University of Pittsburgh.
Experiment 1A determined the effects of overnight water deprivation on fluid ingestion. Eight rats were given ad libitum access to Purina chow powder and water for 1 wk to accustom them to the special cages in which the behavioral measurements were made (25). On the front of these cages a 4 x 4-cm opening had been made to accommodate a jar containing powdered food. The water bottle was supported by a rack on the back of the cage. The drinking spout was recessed 
0.5 cm from the cage, and the rat had access to water by licking through a slot in the cage wall. Licks on the drinking spout activated a contact circuit and were transmitted to a microprocessor and recorded in consecutive 6-s time bins throughout the 1-h sessions. Experimental observations were made during a 20-day period in which rats were deprived of fluid each night from 5:00 PM to 9:00 AM. On the following morning a 1-h drinking session began. Before this session, the food was removed and a fresh solution was made available. Deionized water was available to the dehydrated rats during the drinking sessions on days 1–4. Over the next 16 days the bottle contained a NaCl solution. Specifically, each rat was given 0.05 M NaCl solution to drink on days 5–8, 0.10 M NaCl solution on days 9–12, 0.15 M NaCl solution on days 13–16, and 0.20 M NaCl solution on days 17–20. At the end of the 1-h sessions, food was returned to the cages, and the drinking fluid remained available until 5:00 PM, when the deprivation period began again.
For each animal on each day, the volume of fluid consumed during the 1-h test session was obtained by weighing the bottle before and after the session; the difference (in grams) was interpreted as the volume ingested (in ml). Intakes at intermediate times were computed by multiplying the ingested volume by the number of licks at each time-segment of interest (i.e., 5, 10, 15, 20, and 30 min) and then dividing that product by the number of licks in each session. Note that these computations assumed that the volume consumed per lick was constant throughout the test session. Results presented are for intakes on the fourth day of exposure to each fluid (i.e., on days 4, 8, 12, 16, and 20).
Experiment 1B used similar procedures in rats maintained in commercial metabolism cages to determine whether urinary excretion influenced fluid ingestion. Intakes by dehydrated rats (n = 7) were not monitored electronically but were recorded manually (±0.1 ml). Urine was collected in calibrated tubes (±0.1 ml) at 30 and 60 min of the test session, and its Na+ concentration was measured (±1 meq/l) using a sodium-sensitive electrode (Beckman Coulter, Synchron EL-ISE model 4410, Brea, CA).
Experiment 2A determined the distribution of ingested fluid in the gastrointestinal tract and blood of rats at the end of the initial drinking bout. In experiment 1A, we found that rats drank steadily for 5–10 min after overnight water deprivation regardless of whether water or 0.05–0.20 M NaCl solution was consumed. Thus we focused our attention on the effects of fluid ingestion for varying periods up to 10 min.
On three successive days, 58 rats were adapted to a 16-h period of fluid deprivation (5:30 PM to 9:30 AM) followed by access to the same one of five fluids for 8 h. The fluids were tap water, 0.05 M, 0.10 M, 0.15 M, or 0.20 M NaCl (n = 12, 8, 7, 17, and 14, respectively). As in experiment 1, food was accessible continuously except during the first hour of these 8-h sessions. On the fourth day, drinking fluid again was removed at 5:30 PM. The following morning, at 9:30 AM, food was removed from the cages, burettes containing one of the five fluids became available, and the room lights were dimmed to encourage drinking. The drinking fluid was colored with a dark green food dye (McCormick & Co., Hunt Valley, MO) that permitted the ingested fluid to be readily visible in the small intestine (see below). The drinking test was terminated in one of two ways. Some rats were allowed to drink until they paused for 10 s and moved away from the drinking tube (thereby suggesting that they were not likely to resume drinking soon; Ref. 16), whereas other rats were allowed to drink for variable amounts of time (15–225 s) before being interrupted by the experimenter. The latter animals were used to provide information on the fate of ingested fluid before the cessation of the initial drinking bout. In either case, rats were killed by decapitation within 10 s after the drinking test ended, and fluid intakes (±0.1 ml) and time spent drinking (±1 s) were recorded.
Trunk blood was collected in ice-cold heparinized tubes (143 USP sodium heparin; Becton Dickinson, Franklin Lakes, NJ) and kept on ice until stomachs and intestines were obtained. The abdomen was opened and hemostats were placed at the junction of the stomach with the pylorus, at the junction of the stomach with the esophagus, and at the most distal site of visible dye in the small intestine, in that order. This portion of the surgical procedure took less than 2 min. Each stomach was removed from the carcass, the intestinal distance containing the dye was measured (±1.5 cm), and the intestine was removed. The excised tissues were stripped of adhering blood vessels and connective tissue, and the stomach contents and small intestines were placed in separate beakers. The beakers were covered with Parafilm until they were placed in an oven and dried to constant weight at 60°C for 1–2 days. Finally, the blood was centrifuged (10,000 g for 5 min at 4°C), plasma was harvested, pNa was measured (±1 meq/l) using the sodium-sensitive electrode mentioned above, and plasma protein concentration was measured (±0.1 g/dl) using a refractometer.
To summarize, our goal was to analyze in each of 58 rats all blood samples for plasma concentrations of Na+ and protein, gastric chyme, and small intestine (separately) for dry matter and water, as well as the intestinal distance traversed by the ingested fluid. These analyses sum to a total of 406 individual measurements, of which 14 were lost due to procedural errors.
Experiment 2B used procedures similar to those described in experiment 2A to determine the distribution of ingested fluid at various times after fluid ingestion ended. More specifically, 20 dehydrated rats were allowed to drink water (n = 8), 0.15 M NaCl (n = 6), or 0.20 M NaCl (n = 6) until they stopped (after 5–8 min), at which time the drinking tube was removed. These rats were killed by decapitation 15, 30, 45, or 60 min after fluid ingestion started. Using the procedures described in experiment 2A, plasma concentrations of Na+ and protein were measured in each blood sample, the amounts of dry matter and water were determined both in gastric chyme and small intestine, and the distance traversed by the ingested fluid in the small intestine was recorded. None of these 140 individual measurements were lost.
Finally, six additional rats, not deprived of water, were killed, and blood samples were taken to obtain control values of plasma Na+ and protein concentrations, for purposes of comparison with the values from the various dehydrated groups. None of these 12 individual measurements were lost.
Calculations
Gastric emptying was computed as the difference between the measured fluid intake and the estimated amount of ingested fluid that remained in the stomach and was expressed as a percentage of the intake. To estimate the amount of ingested fluid that remained in the stomach, it was necessary to distinguish that fluid from water already present in the gastric chyme. To address this issue, we evaluated the gastric chyme of water-deprived rats not allowed access to drinking fluid and found that a consistent amount of water was associated with dry matter. Specifically, 12 other rats were trained as above, but on the test day they were denied access to drinking water before they were decapitated; their blood, stomachs, and small intestines were removed and treated as described in Experiment 2A. On the basis of a post hoc evaluation of the obtained data, two scatterplots of the stomach liquids of individual animals (in ml, on the y-axis) expressed as a function of stomach solids (in g, on the x-axis) were prepared, one from rats whose gastric solids were <0.60 g (n = 6) and one from rats whose gastric solids were >0.60 g (n = 6). The associated trendlines, y = 1.3534 x +0.2941 (r = 0.99, P < 0.001) and y = 0.887 x +0.6676 (r = 0.92, P < 0.001), respectively, were used to correct for the amount of fluid associated with gastric solids in each rat tested. That amount was subtracted from the observed water content of the chyme of rats allowed to drink to compute the volume of ingested water that had not yet emptied from the stomach. Forty-two dehydrated rats in experiment 2A had <0.60 g of dry matter in their stomachs, whereas 16 had >0.60 g; thus the "corrected" volumes subtracted from measured gastric water were, at most, only 1.1 ml or 1.8 ml, respectively. Note that these calculations assumed that food residues present in gastric chyme at the start of the drinking test remained in the stomach during the brief period of testing.
Statistical Analysis
All data are presented in scatterplots or as means ± SE. Statistical reliability of observed differences in ingestive behavior was determined by using matched Student's t-tests of mean values. Regression equations were calculated by the method of least squares. P < 0.05 was considered to be statistically significant.
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RESULTS |
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After 16 h of water deprivation, rats drank more or less continuously during the first 5–10 min that water or NaCl solution was accessible. Neither the mean amounts consumed in this first drinking bout (range: 7.7–9.8 ml) nor the latencies to initiate a second bout (range: 10.3–24.6 min) differed significantly as a function of which fluid was consumed (Table 1). Cumulative intakes of the five fluids at 5, 10, 15, and 20 min of the test session were not statistically significant from one another (Fig. 1). During the remainder of the 1-h test session, rats consumed little when they drank water or 0.05 M NaCl and more when they drank 0.10 M, 0.15 M, or 0.20 M NaCl (Fig. 1; all P values <0.05). As shown in Table 1, the mean number of additional drinking bouts ranged from 1.1 (when rats drank water) to 3.4 (when they drank 0.15 M NaCl). The mean amounts consumed in those additional drinking bouts ranged from 0.9 ml (of water) to 3.7 ml (of 0.20 M NaCl) and increased progressively in proportion to the concentration of the ingested fluid (r = 0.97, P < 0.001). In other words, when water was available, rats returned to drink least often and drank the smallest volumes in these later bouts, whereas when 0.15 M or 0.20 M NaCl was available rats returned to drink most often and drank the largest volumes of fluid in those bouts.
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A separate group of dehydrated rats was studied similarly, but this time, excreted urine was collected during the 1-h test session, and its volume and Na+ concentration were measured. The animals drank an average of 8–12 ml in 15 min and 12–17 ml in 60 min, as in experiment 1A, yet few rats voided any urine. Rats drinking 0.20 M NaCl excreted urine in the greatest volumes and highest Na+ concentrations (0.5 ± 0.2 ml in 60 min, 275 ± 12 meq/l).
Experiment 2A
These investigations focused on drinking that occurred during the first 10 min or less of fluid access after overnight deprivation. Seventeen of the 58 rats studied were killed as soon as they ended the first drinking bout whereas the others were interrupted at predetermined times and killed earlier (<5 min after they began to drink). Fig. 2 displays a scatterplot of cumulative intakes of each animal as a function of time spent drinking, and indicates that the dehydrated rats drank at a similar rate over time regardless of which fluid was ingested.
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5 min), the composition of the ingested fluid was found to influence the pNa but not the plasma protein concentration. As indicated in Table 2, the pNa in the seven rats consuming water, 0.05 M, or 0.10 M NaCl was significantly lower than the pNa in the 10 rats consuming 0.15 M or 0.20 M NaCl or the pNa in the 10 rats that were denied access to drinking fluid (both P values <0.01). In contrast, the volumes consumed by rats ingesting water or hypotonic saline were not significantly different from values of rats ingesting isotonic or hypertonic saline. When drinking was interrupted after 3 min, the pNa of rats consuming water or hypotonic saline (144.4 ± 0.2 meq/l after rats drank 4.7 ± 0.5 ml in 2.7 ± 0.3 min, n = 16) also were significantly lower than the values of dehydrated rats not allowed access to drinking fluid (148.3 ± 0.5 meq/l, n = 10, P < 0.001) and of rats consuming isotonic or hypertonic saline (146.1 ± 0.7 meq/l after rats drank 4.5 ± 0.5 ml in 2.9 ± 0.2 min, n = 12, P < 0.05).
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Additional dehydrated rats were killed at various times after an initial drinking bout of water, 0.15 M NaCl, or 0.20 M NaCl. The amounts of ingested fluid found in the stomach and small intestine diminished rapidly with time in each case (Fig. 8). Gastric emptying of water or 0.15 M NaCl was 90–100% by 30–45 min, but it was somewhat slower in rats that drank 0.20 M NaCl (80–90% by 45–60 min). The ingested fluid traveled 90–105 cm into the small intestine by 30 min; >60% of ingested water or 0.15 M NaCl was absorbed by then, whereas absorption of 0.20 M NaCl was slower (60% by the end of the 60-min test period). As shown in Table 2, plasma Na+ was significantly reduced after 15–60 min when rats drank an initial bout of water (140.5 ± 0.4 meq/l, compared with 143.7 ± 0.9 meq/l in nondeprived control rats, n = 6, P < 0.02), but it remained elevated when they drank the saline solutions (146.2 ± 0.6 meq/l, P < 0.05 compared with nondeprived control rats). In contrast, plasma protein concentrations were reduced to levels that were slightly above normal (6.4 ± 0.1 g/dl in rats drinking water and 6.3 ± 0.1 g/dl in rats drinking saline, compared with 6.1 ± 0.1 g/dl in non-deprived control rats, n = 6; P = ns, ns, respectively).
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DISCUSSION |
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The main goal of the present studies was not to determine why the dehydrated rats started to drink but why they stopped. The results displayed in Fig. 1 indicate that the initial drinking bout ended within 10 min whether water or NaCl solution was consumed. When the rats drank water, it was noteworthy that pNa had returned to normal by the time they stopped drinking (Table 1), in confirmation of previous findings (14, 16, 29). However, plasma protein concentration had not changed at this time; that is, the dehydrated animals remained hypovolemic, as expected since most of the ingested water that emptied from the stomach and was absorbed should have entered tissue cells by osmosis. Thus the rats did not stop drinking because of the removal of all excitatory signals for thirst but because of some inhibitory signal that prevailed despite continued plasma volume deficits. The inhibition of thirst that occurs when hypovolemic rats drink water is a well-known phenomenon that has been attributed to osmotic dilution of body fluids (27). However, such inhibition did not appear to be a factor in the present study because osmotic dilution of systemic blood was not evident at the time rats stopped drinking water (although it did occur later; Table 2, also Refs. 14 and 16). Furthermore, the dehydrated rats ended their initial drinking bout at more or less the same time regardless of which fluid they consumed (Fig. 1), and no decrease in pNa was expected or observed in rats that drank 0.15 M or 0.20 M NaCl solution. Thus, in considering the signals that provided the inhibition of thirst, we focused our considerations on the volume of the ingested fluid rather than its concentration.
Thrasher and colleagues (32) have reported that fluid volume ingested by dehydrated dogs is sensed by oropharyngeal receptors that monitor swallowing. These signals inhibited intake after a few minutes of drinking despite the fact that systemic pOsm was not restored until 30 min after water consumption began. Oropharyngeal signals also provided rapid inhibition of the complementary secretion of VP that occurred during dehydration (32). Subsequent studies extended these latter observations to other experimental subjects, including sheep, monkeys, and humans (3, 5, 13). However, we recently reported that the same mechanism does not operate in rats (17, 29). Dehydrated rats, like dogs, began to reduce plasma levels of VP after a few minutes of water consumption, but, unlike dogs, they did not do so when the ingested fluid drained through an open gastric fistula (29). In further contrast with dehydrated dogs, plasma levels of VP were not rapidly reduced when thirsty rats consumed isotonic NaCl solution (17, 29). These findings complement previous reports that drinking is quickly inhibited when a gastric water load is given to dehydrated rats (1) and that dehydrated rats with an open gastric fistula continue to drink water for many minutes (10, 33), unlike dehydrated dogs (1, 32).
The inhibition of thirst that occurs when dehydrated animals drink water was a subject of considerable inquiry before Thrasher et al. (32) reported their seminal findings. Rats were the experimental subject in many of those earlier studies, most of which focused on the roles of gastric distension and systemic hydration in inhibiting water ingestion by dehydrated rats (6). For example, observations that water consumption increased when a closed pyloric cuff precluded gastric emptying (9, 15) suggested that drinking was inhibited under normal conditions by gastric distension together with a signal related to the low osmolality or Na+ concentration of the fluid that entered the small intestine (4, 19). But why do dehydrated rats stop drinking 0.15 M NaCl, when osmotic dilution cannot be a factor? The present results suggest that the inhibitory signal was not provided by gastric distension alone because ingested fluid emptied from the stomach so rapidly; indeed, almost half of it had left the stomach while the dehydrated rats were drinking. Most of that emptied fluid had not yet been absorbed and thus was still present in the small intestine when the animals stopped drinking. Consequently, the sum of gastric and small intestinal volumes after the initial drinking bout was well correlated with fluid intake (Fig. 6). These results allow the hypothesis that the signal inhibiting the initial bout when rats drank 0.15 M NaCl was provided by distension of both the stomach and small intestine. That same signal presumably contributed to inhibition when rats drank the more dilute solutions, together with an additional inhibitory signal related to the dilute concentration of the fluid passing through the small intestine.
Distension of the stomach and small intestine has been proposed to contribute an inhibitory stimulus in the control of food intake when rodents consume liquid diet (12, 22). Consistent with that hypothesis and of clear relevance to our present proposal, stretch receptors on the wall of the stomach and the proximal small intestine allow the detection of distension (18, 34). Because vagal and spinal afferents from these sites project to the nucleus of the solitary tract (NTS) and area postrema (20), it seems plausible that these peripheral nerves project to the same cells (or to neurally linked cells) in the caudal brain stem and in that way contribute to an integrated message. If so, then damage to the afferent fibers or to their projection sites should remove this inhibition and thereby increase fluid ingestion in an initial bout of drinking by thirsty rats. Reports published previously are consistent with this hypothesis. Thus, after systemic injection of capsaicin to destroy visceral sensory nerves with unmyelinated axons, rats showed increased drinking responses to treatments that increase pOsm or decrease plasma volume (7). A similar increase in water consumption has been reported in thirsty rats with aspiration lesions of the area postrema and subadjacent NTS (8). Note that such results would not be expected if cessation of thirst was mediated solely by cerebral osmoreceptors that detected dilution of systemic blood.
The volume of ingested fluid found in the small intestine increased in proportion to intake regardless of which fluid was consumed. It quickly traveled deep into the small intestine, but the distance reached an asymptote at 60–80 cm, which is about two-thirds of the full length of the small intestine in these rats. Presumably, the initial phase of this logarithmic function was due to the propulsion of fluids into the small intestine that resulted from gastric contractions, whereas that high rate of movement slowed, in part, because of resistance encountered as the luminal fluid approached the ileal-cecal sphincter. In addition, the distensible intestinal wall was visibly expanded by the increased luminal fluid, which would slow intestinal transit. The equation for the regression line in Fig. 7, y = 0.010x + 0.015, indicates that the mean distension of the dye-colored segment of small intestine doubled when 1.5 ml of volume entered the intestine. That volume was associated with intakes of 8 ml (Fig. 4), which were the amounts consumed by dehydrated rats after drinking for 5 min (Fig. 2).
After a large initial drinking bout, dehydrated rats consumed a few smaller bouts of additional fluid when they drank the more concentrated NaCl solutions instead of water or 0.05 M NaCl. Note that 8 ml of 0.20 M NaCl, when fully equilibrated with body fluids, is estimated to raise pOsm in these dehydrated rats by only 1 mosmol/kgH2O, which should not make them much thirstier. But what makes them less thirsty and thereby limits their fluid consumption? Because none of these rats excreted much urine during the 60-min period of observation, and plasma Na+ values were little changed after 15–60 min of drinking 0.15 M or 0.20 M NaCl (Table 2), it seems likely that their fluid intakes were not influenced by renal function; in fact, previous studies have shown that dehydrated rats drinking 0.15 M NaCl do not excrete concentrated urine until later (14, 28). Instead, the present results suggest that an early inhibition of thirst occurred because of increased gastrointestinal distension when dehydrated rats drank 0.10–0.20 M NaCl and that this inhibition diminished during the 1-h test period, as ingested fluid was gradually absorbed from the small intestine, which presumably allowed drinking to resume intermittently.
To summarize, dehydrated rats did not continuously ingest fluid until they were fully rehydrated. The early inhibitory signal appears to be related to the volume of ingested fluid rather than to its composition. This volume was highly correlated with the fluid volumes found in the stomach and small intestine of rats when they stopped drinking an initial bout. Thus gastrointestinal distension might plausibly provide an early signal inhibiting thirst in dehydrated rats. According to this hypothesis, gastric emptying would not reduce this putative inhibitory signal as long as the emptied fluid remained in the small intestine. However, the movement of osmolytes into the small intestine can rapidly affect body fluid osmolality, which should decrease the excitatory signals of thirst and thereby limit additional fluid consumption. For example, when dehydrated rats drank water or 0.05 M NaCl, the relatively large osmotic component of the excitatory signal was reduced as body fluids were diluted. Conversely, when dehydrated rats drank 0.15 M or 0.20 M NaCl, absorption of ingested fluid from the small intestine apparently increased plasma volume and thereby reduced the relatively small hypovolemic component of the excitatory signal. In the latter situation, the rats presumably resumed drinking as GI Fill diminished because the large excitatory signal associated with increased pOsm was not affected rapidly. Subsequent investigations must further evaluate whether observed correlations between fluid ingestion and postingestional variables reflect causal relations as proposed.
Perspective
Drinking by dehydrated dogs generates an early oropharyngeal signal that inhibits both thirst and VP secretion (32). The present results, together with earlier observations (29), indicate that the same arrangement does not apply to dehydrated rats. There is an early inhibition of thirst and VP secretion in rats, but the same signal does not inhibit both responses nor is either signal oropharyngeal. This difference between the two species may result from the fact that rats drink relatively slowly but empty ingested fluid from their stomachs relatively quickly compared with dogs. Note that the early inhibition of VP secretion in dehydrated rats, generated once the ingested fluid reaches the small intestine, is more appropriately based on the concentration of the ingested fluid rather than its volume because the fluid need of these animals is largely osmoregulatory. It will be interesting to determine whether early signals inhibit VP secretion and thirst in rats during hypovolemia, and if so, whether they are based on the volume or composition of ingested fluid.
It will also be interesting to determine whether presystemic signals inhibit salt appetite in rats, which is another important homeostatic response to hypovolemia (30). In this regard, recent studies have indicated that when hypovolemic rats were allowed access to water, 0.15 M NaCl, or 0.30 M NaCl in one-bottle tests, intake appeared to be inhibited by two variables, altered pOsm (when the rats drank water or 0.30 M NaCl) and GI Fill (24). Those preliminary findings, together with the present data on fluid ingestion after dehydration, collectively support the hypothesis that GI fill inhibits drinking in rats regardless of whether thirst or salt appetite motivates intake and regardless of what fluid the rats consume.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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REFERENCES |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONREFERENCES |
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