NaCl In Rats Research Articles

Cyclic-AMP regulates postnatal development of neural and behavioral responses to NaCl in rats.

During postnatal development rats demonstrate an age-dependent increase in NaCl chorda tympani (CT) responses and the number of functional apical amiloride-sensitive epithelial Na+ channels (ENaCs) in salt sensing fungiform (FF) taste receptor cells (TRCs). Currently, the intracellular signals that regulate the postnatal development of salt taste have not been identified. We investigated the effect of cAMP, a downstream signal for arginine vasopressin (AVP) action, on the postnatal development of NaCl responses in 19–23 day old rats. ENaC-dependent NaCl CT responses were monitored after lingual application of 8-chlorophenylthio-cAMP (8-CPT-cAMP) under open-circuit conditions and under ±60 mV lingual voltage clamp. Behavioral responses were tested using 2 bottle/24h NaCl preference tests. The effect of [deamino-Cys1, D-Arg8]-vasopressin (dDAVP, a specific V2R agonist) was investigated on ENaC subunit trafficking in rat FF TRCs and on cAMP generation in cultured adult human FF taste cells (HBO cells). Our results show that in 19–23 day old rats, the ENaC-dependent maximum NaCl CT response was a saturating sigmoidal function of 8-CPT-cAMP concentration. 8-CPT-cAMP increased the voltage-sensitivity of the NaCl CT response and the apical Na+ response conductance. Intravenous injections of dDAVP increased ENaC expression and γ-ENaC trafficking from cytosolic compartment to the apical compartment in rat FF TRCs. In HBO cells dDAVP increased intracellular cAMP and cAMP increased trafficking of γ- and δ-ENaC from cytosolic compartment to the apical compartment 10 min post-cAMP treatment. Control 19–23 day old rats were indifferent to NaCl, but showed clear preference for appetitive NaCl concentrations after 8-CPT-cAMP treatment. Relative to adult rats, 14 day old rats demonstrated significantly less V2R antibody binding in circumvallate TRCs. We conclude that an age-dependent increase in V2R expression produces an AVP-induced incremental increase in cAMP that modulates the postnatal increase in TRC ENaC and the neural and behavioral responses to NaCl.

Temporal and qualitative dynamics of conditioned taste aversions in C57BL/6J and DBA/2J mice self-administering LiCl

Self-administration of LiCl solution has been shown to result in the formation of a conditioned taste aversion (CTA) that generalizes to NaCl in rats. This paradigm may have considerable ecological validity as it models CTA learning in natural settings, and also allows for the investigation of drinking microstructure as an assay of potential shifts in stimulus palatability. We used this paradigm to examine possible mouse strain differences in CTA acquisition, generalization, and extinction. In the first experiment, C57BL/6J (B6) and DBA/2J (D2) mice self-administered LiCl (or control NaCl) over a 20-minute free access acquisition period and were tested on the following day with a panel of taste solutions available in brief (5-s) trials delivered in random order. In the second experiment, mice again self-administered LiCl or NaCl (at low, 0.12M, or high, 0.24M concentrations) in a 20-minute session, and on the following day received a 20-minute free access period to equimolar NaCl. Strain differences were found for aspects of ingestive behavior, with B6 mice showing greater consumption of all stimuli, including water, while D2 mice lick faster, in less frequent but longer bursts. We did not, however, find evidence of a robust strain difference in taste aversion learning. Both strains demonstrated profound alterations in licking microstructure in the generalization session relative to controls. We suggest that a decrease in “lick efficiency” (the percentage of inter-lick intervals within a burst of short duration vs. longer duration) reflects avoidance behavior, and signals a shift in palatability of a stimulus following CTA.

Dynamics of cognitive disturbances in rats with acute cerebral ischemia on the background of introduction of 0.9 % solution NaCl

For today there are no clear recommendations on infusion therapy at the disease and injuries of brain, and infusion preparations are commonly used empirically. Within the framework of the complex study of an influence of the different infusion remedies on brain at an experimental ischemia of brain, an aim of this work is to investigate how the 0,9 % solution of NaCl influences on the dynamics of cognitive functions and neurological status of the rats with an acute cerebral ischemia at the course medical introduction into an animal organism. Methods . Experiments were carried out on 60 white rats-males. An acute disturbance of cerebral blood circulation (ADCBC) was modeled by means of the two-sided dressing of internal carotid arteries. The 0,9 % solution of NаСІ was injected intravenously in catheterized thigh vein 2,5 ml/kg 2 times/day (5 ml/kg for a day). The first introduction was carried out in 30 minutes after ADCBC and then every day in 12 hours during 7 days. The control groups consist of intact rats that received 0,9 % NаСІ and animals with a model ischemia without treatment. Neurological deficiency in animals was defined on the scale stroke-index McGrow C. P. The dynamics of position-finding activity was assessed in experiment “an open field”. An assessment of animal capacity to training and memorization of an aversive stimulus was studied in the test of conditioned response of passive avoidance. The results were processed using the program StatPlus 2009. Results . The study showed that bilateral carotid occlusion in rats without treatment is followed not only by the high animal lethality but also by the development of a hard neurological symptomatology and then by essential disturbance of mnestic functions in animals that survived during the recovery period of model insult (р<0,01). The study of lethality dynamics, neurological status, behavioral responses in rats with ADCBC on the model of bilateral carotid occlusion showed that the course therapeutic infusion of 0,9 % solution of NaCl had some advantages relative to the group of the control pathology on indicators of neurological deficiency, orientating and searching activity, capacity to training and memorization. Conclusions. Infusion therapy with 0,9 % solution of NaCl in rats with the model cerebral ischemia in some degree promotes the renewal of its cognitive functions (р<0,05) relative to the untreated animals. Therapeutic effect of infusion therapy obtained in experiment with isoosmolar 0,9 % solution of NaCl is a reason to study protective actions of infusion preparations of the other groups at an acute disturbance of cerebral blood circulation

Importance of the Infusion Rate for the Plasma Expanding Effect of 5% Albumin, 6% HES 130/0.4, 4% Gelatin, and 0.9% NaCl in the Septic Rat*

To compare the plasma volume (PV) expanding effect of a fast infusion rate with that of a slow infusion rate of a fixed volume of 5% albumin, of the synthetic colloids, 6% hydroxyethyl starch 130/0.4 and 4% gelatin, and of 0.9% NaCl in a rat sepsis model and to compare the plasma-expanding effect among these fluids. Prospective, randomized animal study. University hospital laboratory. One hundred and twelve adult male rats. Sepsis was induced by cecal ligation and incision followed by closure of the abdomen. After 3 hrs, an infusion of the PV expander under study was started at a volume of 12mL/kg for the colloids and of 48mL/kg for 0.9% NaCl, either for 15 mins or for 3 hrs. A control group underwent the same experimental procedure but no fluid was given. Three hours after start of the infusion (end of experiment), the plasma-expanding effect was better with a slow than a fast infusion rate for the colloids, especially albumin, but the NaCl groups did not differ significantly from the control group. The PV for the control group was 28.7±3mL/kg. In the slow and the fast infusion groups, it was 38.9±4.3 and 32.6±4.2mL/kg for albumin (p < 0.001), 32.9±4.3 and 29.5±4.4mL/kg for hydroxyethyl starch 130/0.4 (p < 0.05), 31.8±3.9 and 28.2±4.1mL/kg for gelatin (p < 0.05), and 31.8±5.3 and 30.7±6.6mL/kg for NaCl (n.s), respectively. The study showed that the PV expansion by a colloid was greater when given at a slow than at a fast infusion rate, an effect more pronounced for albumin. This difference was not seen for NaCl. The PV-expanding effect was poor for NaCl and better for albumin than for the other colloids.

Dietary sodium deprivation reduces gustatory neural responses of the parabrachial nucleus in rats

Acute sodium depletion induced by furosemide reduces gustatory responses of parabrachial nucleus (PBN) neurons to 0.3-0.5M NaCl in rats. However, in the rat nucleus of the solitary tract (NST), where taste-responsive cells project to the PBN, acute sodium depletion and dietary sodium deprivation elicit different response profiles to lingual NaCl stimulation. To examine the effect of dietary sodium deprivation on the responses of PBN gustatory neurons, we observed the taste responses of the PBN neurons to the four taste qualities and serial concentrations of NaCl in 15-day dietary sodium-deprived and control rats. The results showed that sodium deprivation reduced the responses of PBN taste neurons to 0.1-1.0M NaCl, but not to other tastants. Based on the analyses classified by best-stimulus categories, the number of NaCl-best neurons decreased from 68% to 45% following dietary sodium deprivation, and the responses of the NaCl-best neurons to 0.03-1.0M NaCl were significantly inhibited. Multidimensional scaling illustrated that sodium deprivation increased the similarity of the response profiles of the NaCl-best neurons. These findings suggest that dietary sodium deprivation might modulate sodium intake via increasing aversive threshold for salt rather enhancing salt discrimination.

Sodium ingestion in oxytocin knockout mice

Under certain circumstances, central oxytocin (OT) pathways inhibit dietary intake of NaCl in rats and mice. C57BL/6 OT knockout (OT KO) mice were reported to consume greater amounts of saline solution than wild type (WT) cohorts when both were water deprived overnight. In this study, we determined that OT KO and WT mice of C57BL/6 strain demonstrate an equivalent taste aversion for continuously available 0.2 M, 0.3 M or 0.5 M NaCl. The aversion was proportional to the concentration of NaCl, similar to what has been reported in rats. Furthermore, OT KO and WT animals ingested the same daily amounts of a low, 0.01%, regular, 1.0%, and a high, 8.0%, NaCl diet that was provided ad libitum as a single choice. While consuming these diets, mice were given the choice to drink water or saline (0.5 M NaCl). As the amount of NaCl in the diet increased, mice of both genotypes significantly decreased the consumption of saline solution to an equal degree. Additionally, in an experimental model of sustained dehydration previously developed in rats, 0.5 M NaCl was the only available drinking fluid. Like rats subjected to this paradigm, OT KO and WT mice decreased food intake, decreased body weight and increased fluid ingestion with no genotypic differences. These findings suggest that oxytocinergic neuronal pathways cannot be the only regulator of ad libitum intake of NaCl in drinking solutions or diet. It appears that OT pathways may be more critical in controlling NaCl intake over brief intervals when an animal is quickly compensating for a dehydrating stimulus.

Effects of Selective Lingual Gustatory Deafferentation on Suprathreshold Taste Intensity Discrimination of NaCl in Rats.

In rats, chorda tympani nerve transection (CTX) greatly increases the detection threshold of sodium chloride (NaCl) and severely disrupts salt discriminability. Here it is shown that CTX has surprisingly little effect, if any, on suprathreshold intensity discrimination. Glossopharyngeal nerve transection (GLX), which has no reported effect on salt sensibility, also did not affect performance. Rats were tested in a 2-response, operant taste intensity discrimination task. Difference thresholds for CTX rats were only slightly higher (-0.15 log/10 unit) than those for GLX and sham-transected rats, when 0.05 M served as the standard, and did not significantly differ when 0.1 M NaCl was the standard. Although the perceived intensity of NaCl might be reduced by CTX, input from remaining taste nerves sufficiently maintains the relative discriminability of suprathreshold NaCl concentrations.

Ethnopharmacological Studies on Allspice (Pimenta dioica) in Laboratory Animals

An aqueous suspension of allspice, Pimenta dioica (L.) Merr. (Myrtaceae), has been studied for antiinflammatory, analgesic, antipyretic, gastric antiulcer, and cytoprotective activities in experimental models. The suspension produced significant inhibition of carrageenan-induced paw edema, cotton pellet granuloma in rats, a significant inhibition of acetic acid-induced writhing and tail flick reaction time and reduction of yeast-induced hyperpyrexia in mice. The suspension also showed antiulcer and cytoprotective activity by protecting gastric mucosa against indomethacin and various necrotizing agents including 80% ethanol, 0.2M NaOH and 25% NaCl in rats. The allspice suspension also increased the gastric wall mucus in rats. Acute toxicity studies showed neither mortality nor adverse effects up to a dose of 7.5 g/kg in mice.

Low environmental temperature modulates gustatory nerve activity and behavioral responses to NaCl in rats.

We studied the effects of cold ambient temperature on chorda tympani nerve responses to taste stimuli such as sucrose, NaCl, quinine HCl (QHCl), and HCl in rats. The electrophysiological recordings of the whole chorda tympani nerves from control (22 degrees C) and cold-exposed (4 degrees C) rats revealed that the responses to sucrose, HCl, and QHCl were unaffected by cold exposure. In contrast, the nerve responses to NaCl were enhanced time dependently, reaching a maximum 7-14 days after cold exposure. Responses to sodium acetate were likewise elevated as they were to NaCl, whereas those to KCl were unchanged after cold exposure. In addition, the residual NaCl responses after lingual application of the sodium-channel blocker amiloride in cold-exposed rats were similar to those in control animals. It is thus most likely that cold exposure potentiates the chorda tympani nerve responses to Na(+), but not to Cl(-). Behavioral studies with the two-bottle preference test showed that the cold-exposed rats refused to drink NaCl solutions at 0.05 and 0.1 M, the concentrations being preferred by control animals. These results suggest that the ambient temperature influences taste cell function, and that the enhanced NaCl response of the chorda tympani nerve is related to the avoidance of NaCl intake under cold environment.

H 2 histaminergic control of inhibition of eating induced by intragastric NaCl in rats

KRALY, F. S., J. B. KATZ, A. E. BURCHARD, C. CASE, V. A. GABRIEL, T. A. LANZ, M. E. MIKKELSEN AND M. B. SOKOL. H 2 histaminergic control of inhibition of eating induced by intragastric NaCl in rats. PHYSIOL BEHAV 65(1) 105–113, 1998.—A role for endogenous histamine and histamine receptor subtypes in mediating the inhibition of eating induced by intragastric (i.g.) hypertonic NaCl was examined in adult male Sprague–Dawley rats surgically equipped with a chronic gastric catheter. The i.g. infusion of 2 mL 900 or 1,800 mOsm/kg of NaCl inhibited: 1) ingestion of pellets in rats eating after 24-h food deprivation; and 2) ingestion of cookies in rats eating without prior deprivation. The H 1 receptor antagonists dexbrompheniramine (DXB; 1 mg/kg) and pyrilamine (PYR; 4 mg/kg) did not attenuate the inhibitory effects of i.g. 900 or 1,800 mOsm/kg of NaCl for rats eating pellets and for rats eating cookies. The H 2 antagonists cimetidine (CIM; 16 mg/kg) and metiamide (MET; 16 mg/kg) attenuated the inhibitory effects of i.g. 1,800 mOsm/kg of NaCl upon ingestion of cookies, but intracerebroventricular (i.c.v.) infusion (through a chronic indwelling cannula) of 100 μg of CIM did not mimic this effect of intraperitoneal (i.p.) CIM. The i.p. CIM failed to attenuate the inhibition of eating cookies produced by i.p. octapeptide of cholecystokinin (CCK-8; 3 μg/kg). The H 3 antagonist thioperamide (TH; 10 mg/kg i.p.) and the H 3 agonist R-α-methylhistamine (RAM; 3 mg/kg i.p.) did not alter the inhibitory effect of i.g. 1,800 mOsm/kg of NaCl for rats eating cookies. Combined treatments of systemic DXB plus CIM, and DXB plus CIM plus thioperamide (TH) did not reverse the inhibitory effects of i.g. 1,800 mOsm/kg of NaCl upon ingestion of cookies. Finally, i.p. DXB, but not CIM, attenuated the ability of i.g. 900 mOsm/kg of NaCl to increase water intake; conversely, i.p. CIM, but not DXB, attenuated the ability of i.g. 900 mOsm/kg of NaCl to inhibit eating of cookies. These findings demonstrate a double dissociation of effects upon ingestive behavior: H 1, but not H 2, antagonism attenuates the effect of i.g. hypertonic NaCl on water intake, whereas H 2, but not H 1, antagonism attenuates the inhibition of eating produced by i.g. hypertonic NaCl. These results demonstrate that different subtypes of peripheral and/or central histamine receptors contribute to different behavioral consequences of postprandial gastrointestinal osmotic loads in rats.

Effects of caffeine on glandular stomach carcinogenesis induced in rats by N-methyl- N′-nitro- N-nitrosoguanidine and sodium chloride

The modifying effects of caffeine ingestion on glandular stomach carcinogenesis induced by N-methyl- N′-nitro- N-nitrosoguanidine (MNNG) and sodium chloride (NaCl) were investigated in male Wistar rats. Animals were given a MNNG solution (100 ppm) as their drinking water and simultaneously fed a diet supplemented with 5% NaCl for 8 wk. They then received 0.25% caffeine solution (groups 1 and 3) or tap water (groups 2 and 4) as the drinking water, and were fed the NaCl diet (groups 1 and 2) or basal diet (groups 3 and 4) for the following 32 wk. Both caffeine and NaCl treatments exerted growth retardation effects, the suppression being stronger with caffeine than NaCl, and animals in group I (NaCl plus caffeine) showing the lowest body weight. The incidence of adenocarcinomas in the pylorus was significantly decreased in group 1 compared with the group 2 (NaCI) value ( P < 0.05). The incidence of atypical hyperplasias in the fundus was also lower in group 1 than in group 2, although in both cases significantly higher ( P < 0.05 and P < 0.01) than in group 4 (no treatment). These results were in good agreement with short-term assay findings whereby lipid peroxidation in the glandular stomach mucosa induced by 4% NaCl ingestion was inhibited by caffeine treatment. In group 3 (caffeine), caffeine intake by itself did not modulate glandular stomach tumour development. The results thus suggest that caffeine inhibits the gastric tumour promotion activity of NaCl in rats.

Inhibition of isotonic sodium chloride intake in the rat by selective tachykinin agonists

The present study investigated the effect of the central injection of selective tachykinin (TK) agonists on the need-free intake of 0.9% NaCl in rats. Isotonic NaCl was offered for 60 min (between 1800 and 1900 h); water was offered for 4 h (between 1800 and 2200 h). The TK agonists were injected into the third ventricle just before access to fluids. The NK 3-selective agonists [Asp 5,6, MePhe 8]substance P(5–11) and Succ[Asp 6,MePhe 8]substance P(6–11), as well as the NK 1-selective agonist [Sar 9, Met(O 2) 11]substance P, markedly reduced salt intake, the threshold dose for their effects being 5 ng/rat. The NK 2-selective agonist GR64349 reduced salt intake only at 500 ng/rat. At the dose of 31.2 ng/rat, neither the NK 1 nor the NK 3 agonists inhibited water intake, when water was the only fluid offered (between 1800 and 2200 h), or modified food intake, but also the need-free food-deprived rats. The present study shows that a) TKs inhibit not only the need-induced salt intake, but also the need-free intake of isotonic saline, b) this effect is behaviorally selective, and c) the effect is apparently mediated by NK 1 and NK 3 receptors. The finding that TKs suppress salt intake in a large variety of experimental conditions supports the idea that the antinatriorexic effect of TKs is independent of the physiological and hormonal status of the animal. It is hypothesized that TKs might modify taste sensitivity or the hedonic evaluation of the salty taste.

Gastric Anti-Ulcer and Cytoprotective Effects of Cyamopsis tetragonoloba (‘Guar’) in Rats

AbstractAn ethanol extract of Cyamopsis tetragonoloba (Guar) has been studied for its ability to inhibit gastric secretion and to protect gastric mucosa against the injury caused by pylorus ligation, hypothermic restraint stress, indomethacin, and various necrotizing agents including 80% ethanol, 0.2 M NaOH and 25% NaCl in rats. An oral dose of 500 mg/kg of the extract produced inhibition of normal gastric secretion in rats. The extract inhibited acetylcholine-induced contractions of isolated guinea pig ileum, suggesting anti-cholinergic activity. The intensity of gastric lesions induced by hypothermic restraint stress and indomethacin was reduced significantly by Guar extract. It produced a marked cytoprotective effect against all the necrotizing agents used in this study. The extract not only increased the gastric wall mucus significantly but also restored the ethanol-induced depletion of nonprotein sulfhydryl (NP-SH) content in the glandular stomachs of rats.

Central γ-aminobutyric acid stimulation attenuates pressor responses to intracisternal injection of hypertonic NaCl in rats

Central γ-aminobutyric acid stimulation attenuates pressor responses to intracisternal injection of hypertonic NaCl in rats

Systemic administration of baclofen inhibits water intake in rats

1. 1. The present experiments were carried out to investigate the effects of systemic administration of baclofen on water intake in rats. 2. 2. Baclofen (1, 2 and 4 mg/kg, s.c.) inhibited water intake in 16 hr water-deprived rats in a dose-related manner, with maximal effects occurring during the first 30 min after administration. 3. 3. Baclofen (0.25 and 2 mg/kg, s.c.) had no effects on water intake in non-deprived rats. 4. 4. Baclofen (2 mg/kg) inhibited water intake elicited by i.p. injection of hypertonic NaCl in rats. 5. 5. Baclofen (1 mg/kg) did not produce taste aversion in a taste aversion experiment. This indicates that the effects of baclofen on water intake is not due to an aversive effect of the drug.

Comparison of preference thresholds for NaCl solution in rats of the Sprague-Dawley and Long-Evans strains

Rats of the Sprague-Dawley and Long-Evans strains were compared with respect to their preference threshold and preference maximum concentrations for NaCl solution in a two-bottle choice paradigm. The preference threshold for NaCl in rats of the Sprague-Dawley strain occurred when the concentration of NaCl presented was 0.030 M. The preference maximum concentration was 0.10 M. In the case of rats of the Long-Evans strain, a preference threshold concentration was not clearly manifested although the preference maximum concentration was also 0.10 M. Thus, the previously reported lack of an appetite for isotonic NaCl solution in rats of the Long-Evans strain compared to those of the Sprague-Dawley strain is most likely related to the failure of rats of the former strain to discriminate between water and NaCl solution until the concentration of NaCl exceeds 0.15 M. However, at this concentration, both strains rejected NaCl solution in favor of water. In contrast to the results with NaCl solution, rats of the Long-Evans strain appear to have a greater appetite for 5% glucose solution than do those of the Sprague-Dawley strain. Whether this is related to a reduced preference threshold concentration for glucose remains to be tested.

Sodium appetite: Species and strain differences and role of renin-angiotensin-aldosterone system

The characteristics of the appetite for NaCl in humans differ in some aspects from those in other species. The mechanisms of appetite for NaCl have been studied in detail in two species, rats and sheep. We review the treatments known to induce an appetite for NaCl in rats, with special reference to differences among strains in their spontaneous preference for NaCl solution. The current view of the mechanism is critically appraised, with particular emphasis on the role of angiotensin II, mineralocorticoids, cerebroventricular sodium transport, and the relation between preference for NaCl and the concentration of sodium in saliva. The appetite for NaCl in rodents other than rats is considered next, and reveals that mice, hamsters and gerbils are reluctant to ingest NaCl either spontaneously or after treatment with several of the natriorexigenic stimuli that are effective in rats. The characteristics of the appetite for NaCl in non-rodent species, including sheep, rabbit, dog, and non-human primates, are then described. We discuss some of the possible differences in mechanism that might account for this behavioral diversity among species.

Epithelial restitution and cellular proliferation after gastric mucosal damage caused by hypertonic NaCl in rats.

Hypertonic NaCl enhances gastric cancer in rats induced by N-nitroso compounds. This study was designed to examine the structural changes and alterations in mitotic activity occurring after mucosal exposure to hypertonic NaCl. Wistar rats were given one ml of 4.5 M NaCl by gastric tube and groups of 4-5 animals were sacrificed at different time intervals up to 120 h. An i.p. injection of thymidine was given 1 h before death. Samples of antral and corpus mucosa were prepared for microscopy and autoradiography. Hypertonic NaCl caused uniform destruction of surface mucous cells and pits in the corpus and antrum. Epithelial restitution with the formation of a thin epithelial layer occurred within one h of damage. The mucosa changed towards normal within 24-48 h. The distance between mucosal surface and the replicating cells decreased during the first 2 h. The proliferation zone remained in the middle of the glandular layer throughout the experiment. The proliferative activity increased during the first 24 h after mucosal damage. The number of labelled cells per unit area of mucosa was somewhat larger in the corpus than the antrum, but in the corpus the distance between proliferating cells and mucosal surface was double that of the antrum. Hypertonic NaCl causes a series of changes in the gastric mucosa. The increased mitotic activity can only partly explain the cocarcinogenic effect, since N-nitroso-induced adenocarcinomas occur predominantly in the antrum while the mitotic activity is maximal in the corpus.

Effect of variation of the composition of CSF in the rat upon drinking of water and hypertonic NaCl solutions.

Infusing conscious unrestrained rats with either 0.5 M NaCl-CSF or 0.7 M sucrose-CSF into the lateral cerebral ventricle (IVT) at 38 microliters/hr for 4 hr induced drinking. Although the infusates were nearly equiosmotic, water drinking during the 0.5 M NaCl-CSF was greater than during 0.7 M sucrose-CSF. However, IVT infusions of 0.7 M mannitol-CSF at rates of 9.4 microliters/hr or 38 microliters/hr for 4 hr or 10 microliters/hr for 4 days failed to induce water drinking. Also, IVT infusion of 0.27 M mannitol-CSF at 38 microliters/hr for 4 hr failed to significantly alter water drinking. CSF [Na] was reduced by IVT infusion of either 0.7 M sucrose-CSF or 0.7 M mannitol-CSF. In contrast, CSF [Na] was increased by 4-hr IVT infusion of 0.5 M NaCl in rats denied access to water during the infusion. Intake of 0.5 M NaCl was not altered significantly from control intakes by any of the above IVT infusions. It is concluded that water drinking in the rat may be initiated by stimulation of either a sodium sensitive sensor alone or with an osmoreceptor system and that species specific differences in the induction of both water drinking and hypertonic saline drinking are apparent.

Pressor responses to intracisternal injection of hypertonic NaCl in rats.

Hypertonic NaCl solution injected into the cisterna magna of anesthetized rats produced dose-dependent pressor responses accompanied by slight tachycardia. Similar injections of hypertonic urea solution were ineffective. Because the early phase of the pressor response to hypertonic NaCl was always accompanied by increased sympathetic nerve firing and was inhibited following alpha-adrenergic blockade with phentolamine, initial pressor response was attributed to sympathetic hyperactivity. On the other hand, because the later phase of the pressor response was unaffected either by adrenalectomy or by alpha-adrenergic blockade, but was significantly inhibited by hypophysectomy or by pretreatment with a vasopressin antagonist, the later pressor response was ascribed to an increased release of endogenous vasopressin. Thus, our findings indicate that central pressor responses to hypertonic NaCl solution involve two different mechanisms: sympathetic hyperactivity in the early phase and vasopressin release during the later phase. In spontaneously hypertensive rats (SHR), both pressor and sympathetic responses to intracisternally injected NaCl were greater than in Wistar-Kyoto rats (WKY). Our results further indicate hypersensitivity to NaCl around the brain stem in SHR, which could account for the increased sympathetic activity and cause SHR to develop hypertension.