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2 Departments of Psychology and Pharmacology and the Cardiovascular Center, University of Iowa, Iowa City, Iowa 52242-1407; and 1 Departamento de Ciências Fisiológicas, Faculdade de Odontologia, Paulista State University, Araraquara, São Paulo 14801-903, Brazil
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ABSTRACT |
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Top
Abstract
Introduction
Materials & Methods
Results
Discussion
References
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The
present study investigated the effects of bilateral injections of the
nonselective CCK receptor antagonist proglumide or CCK-8
into the lateral parabrachial nuclei (LPBN) on the ingestion of 0.3 M
NaCl and water induced by intracerebroventricular
injection of ANG II or by a combined treatment with subcutaneous
furosemide (Furo) + captopril (Cap). Compared with the
injection of saline (vehicle), bilateral LPBN injections of proglumide
(50 µg · 200 nl
1 · site1)
increased the intake of 0.3 M NaCl induced by intracerebroventricular ANG II (50 ng/1 µl). Bilateral injections of proglumide into the LPBN
also increased ANG II-induced water intake when NaCl was simultaneously
available, but not when only water was present. Similarly, the
ingestion of 0.3 M NaCl and water induced by the treatment with Furo
(10 mg/kg) + Cap (5 mg/kg) was increased by bilateral LPBN proglumide
pretreatment. Bilateral CCK-8 (0.5 µg · 200 nl1 · site1)
injections into the LPBN did not change Furo + Cap-induced
0.3 M NaCl intake but reduced water consumption. When only water was available after intracerebroventricular ANG II, bilateral LPBN injections of proglumide or CCK-8 had no effect or significantly reduced water intake compared with LPBN vehicle-treated rats. Taken
together, these results suggest that CCK actions in the LPBN play a
modulatory role on the control of NaCl and water intake induced by
experimental treatments that induce hypovolemia and/or hypotension or that mimic those states.
sodium chloride intake; water intake; proglumide; sodium appetite
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INTRODUCTION |
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Top
Abstract
Introduction
Materials & Methods
Results
Discussion
References
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THE LATERAL PARABRACHIAL nucleus (LPBN) has been identified as an important site involved in the control of water and NaCl intake in rats (6, 17, 18, 20, 21). This hindbrain structure is reciprocally connected with several forebrain areas, such as the paraventricular nucleus of the hypothalamus, central nucleus of the amygdala, bed nucleus of the stria terminalis, and median preoptic nucleus, that are associated with the control of fluid intake and electrolyte balance (5, 14, 16, 22, 24). Also the LPBN receives afferent projections from more caudal regions, such as the area postrema (AP) and the medial portion of the nucleus of the solitary tract (mNTS; 9, 13, 15), that have also been implicated in the control of NaCl and water intake in rats (7).
Recent studies (6, 18) have shown that bilateral LPBN injections of methysergide, a serotonergic receptor antagonist, markedly increase NaCl intake induced by ANG II administered either intracerebroventricularly or into the subfornical organ. NaCl intake induced by combined treatment with the diuretic furosemide (Furo) and the angiotensin-converting enzyme inhibitor captopril (Cap) was also increased after bilateral LPBN methysergide injection and decreased after injection of a serotonergic receptor agonist, (±)-2,5-dimethoxy-4-iodoamphetamine hydrochloride, into the same loci (18). These results suggest that serotonergic mechanisms in the LPBN modulate sodium intake induced by central ANG II or by the treatment with Furo + Cap. The presence of a prominent serotonergic pathway from the AP to the parabrachial nucleus (15) raises the possibility that information carried from the AP to the LPBN participates in the control of NaCl intake.
Feeding studies suggest that the peptide CCK inhibits the ingestion of food through actions on central structures (8, 10, 28). CCK has been demonstrated to be present in the LPBN (3), and the projection from the LPBN to ventromedial hypothalamic nucleus may be important for the satiety induced by CCK (12, 28). CCK injections into the hypothalamus, medial pontine area, and nucleus of the solitary tract (NTS) reduce food intake (25). An interaction between CCK and serotonin (5-HT) in the control of ingestive behavior has also been suggested (8). It is of interest that there is a CCK pathway originating in the NTS that projects to the LPBN (13). Because of similarities in the roles of 5-HT and CCK on feeding, we have investigated the effects of bilateral LPBN injections of CCK-8 or of the nonselective CCK receptor antagonist proglumide on experimentally induced thirst and salt appetite.
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MATERIALS AND METHODS |
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Top
Abstract
Introduction
Materials & Methods
Results
Discussion
References
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Animals
Male Sprague-Dawley rats (Harlan, Indianapolis, IN) weighing 300-400 g were used. The animals were housed in individual stainless steel cages with free access to normal sodium diet (Purina rat chow 5012), water, and 0.3 M NaCl solution.Cerebral Cannulas
Rats were anesthetized with 0.33 ml/100 g body wt of an anesthetic solution (similar to the commercial anesthetic Equithesin) composed of 0.97 g of pentobarbital sodium and 4.25 g of chloral hydrate/100 ml distilled water (prepared by the Pharmacy Department, The University of Iowa Hospitals and Clinics) and placed in a Kopf stereotaxic instrument. The skull was leveled between bregma and lambda. Stainless steel 23-gauge cannulas were implanted bilaterally into the LPBN using the coordinates 9.4 mm caudal to bregma, 1.9 mm lateral to the midline, and 4.1 mm below the dura. The tips of the cannulas were positioned at points 2 mm above the LPBN. In some of the rats, a third cannula was implanted in the left lateral ventricle (LV) using the coordinates 1.2 mm caudal to bregma, 1.5 mm lateral to the midline, and 4.0 mm below the dura mater. The cannulas were fixed to the cranium using dental acrylic resin and jewelers' screws. A 30-gauge metal obturator filled the cannulas, except during injections.Drugs
Furo (Elkins-Sinn, Cherry Hill, NJ) was administered subcutaneously at 10 mg/kg body wt. Cap (SQ-14,225), a gift from E. R. Squibb & Sons (Princeton, NJ), was dissolved in sterile isotonic saline immediately before each experiment and injected subcutaneously at 5 mg/kg body wt. ANG II (acetate salt, human, synthetic) was purchased from Sigma Chemicals (St. Louis, MO), and proglumide sodium salt and CCK-8 sulfated (cholecystokinin fragment 26-33) were purchased from Research Biochemical International (Natick, MA). All drugs for central injections were dissolved in isotonic saline.General Procedures
Rats were tested in their home cages. Water and 0.3 M NaCl were provided from burettes with 0.1-ml divisions that were fitted with metal drinking spouts. Water and 0.3 M NaCl intakes were induced by intracerebroventricular injection of ANG II (50 ng/1 µl) or by treatment with subcutaneous Furo (10 mg/kg body wt) + Cap (5 mg/kg body wt) as described previously (11, 29). Injections into the LPBN and LV were performed using 10-µl Hamilton syringes connected by polyethylene tubing (PE-10) to 30-gauge injection cannulas. The injection cannulas were 2 mm longer than the guide cannulas. The injection volumes were 200 nl for LPBN and 1 µl for the LV.Experimental Protocols
In the following experimental protocols, each rat received no more than four tests and a period of at least 3 days intervened between tests. In each experimental session, except as noted, one-half of the rats received bilateral injections of vehicle into the LPBN and the remaining animals received injections of CCK-8 or proglumide into the LPBN (i.e., a randomized design).Protocol 1: Effects of bilateral LPBN proglumide
injections on intracerebroventricular ANG II-induced 0.3 M NaCl and
water intakes. ANG II was injected into the LV 10 min
after bilateral LPBN injections of either vehicle (isotonic saline 200 nl/site) or 50 µg proglumide · 200 nl1 · site1.
After the ANG II injection, the volumes of 0.3 M NaCl and water ingested were measured at 15-min intervals over a 1-h period.
As a follow-up to the randomized test, a subset of animals was randomly
selected and given 10 µg proglumide · 200 nl1 · site1
before intracerebroventricular ANG II.
Protocol 2: Effects of bilateral LPBN proglumide
injections on Furo + Cap-induced 0.3 M
NaCl and water intake. Rats received Furo + Cap
treatments and were returned to their home cages in the absence of NaCl
solution and water. Fifty minutes later, the animals received bilateral
LPBN injections of either vehicle (isotonic saline 200 nl/site) or
proglumide (50 µg · 200 nl1 · site1).
Ten minutes later, access to 0.3 M NaCl and water was restored. The
intakes of these fluids were then recorded every 30 minutes for the
next 2 h.
Protocol 3: Effects of bilateral LPBN CCK-8 injections
on Furo + Cap-induced 0.3 M NaCl and
water intake. Rats received Furo + Cap treatments and
were returned to their home cages where water and 0.3 M NaCl were
removed. Fifty minutes later, the animals received bilateral LPBN
injections of either vehicle (isotonic saline 200 nl/site) or CCK-8
(0.5 µg · 200 nl1 · site1).
Ten minutes later, 0.3 M NaCl and water were returned to the cages and
the volumes of the two fluids were recorded every 30 minutes for the
next 2 h.
Protocol 4: Effect of bilateral LPBN proglumide
injections on ANG-induced water intake. To assess
whether LPBN-injected proglumide had any effect on ANG-induced water
intake when only water was available, ANG II was injected into the LV
10 min after bilateral LPBN injections of either vehicle (isotonic
saline 200 nl/site) or 10 µg proglumide · 200 nl1 · site1
(order randomized). Immediately after the ANG II injection, only water
was available and intake was measured at 15-min intervals over a 1-h
period.
As a follow-up a few days after the last of the two tests, a randomly selected subset of the group of animals was given 50 µg proglumide/200 nl saline at each LPBN site before intracerebroventricular ANG II.
Protocol 5: Effect of bilateral CCK-8 injections on
ANG-induced water intake. To assess whether
LPBN-injected CCK-8 had any effect on ANG-induced water intake when
only water was available, the procedures described in
protocol
4 were followed except that animals
received bilateral LPBN pretreatment with vehicle (isotonic saline 200 nl/site) or 0.1 µg CCK-8 · 200 nl1 · site1
rather than proglumide.
Protocol 6: Effect of bilateral LPBN proglumide
injections in the absence of a
natriorexigenic-dipsogenic
treatment. Animals were given access to 0.3 M NaCl and
water immediately after bilateral LPBN injections of 50 µg
proglumide · 200 nl1 · site1
and intakes were measured for the next 120 min.
Histology
At the end of the experiments, the animals received bilateral injections of methylene blue solution (200 nl) into each LPBN. They were then deeply anesthetized with pentobarbital sodium (80 mg/kg) and perfused transcardially with saline followed by 10% Formalin. The brains were removed, fixed in 10% Formalin, frozen, cut in 50-µm sections, stained with cresyl violet, and analyzed by light microscopy to confirm the injection sites in relation to the LPBN and LV.Statistical Analysis
The results are reported as means ± SE. Repeated-measures analysis of variance was performed to determine overall main effects. In the treatments where ANOVAs showed a significant main effect and/or interaction, follow-up tests were conducted using Fisher's least-significant difference (LSD) test. Differences were considered significant at P < 0.05.| |
RESULTS |
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Top
Abstract
Introduction
Materials & Methods
Results
Discussion
References
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Histological Analysis
As shown in Fig. 1, typical LPBN injection sites were centered in the central lateral and the dorsolateral portions of the LPBN. The injection sites that were judged to terminate in the LPBN were comparable to those reported in other recent studies (6, 17, 18) from our laboratory. As indicated from the spread of methylene blue, injections normally reached the ventral lateral and external lateral portions of the LPBN. In some animals, the injections reached the Kölliker-Fuse (KF) nucleus and the results from these rats were also included in the analysis. The KF nucleus has been traditionally considered to be a ventrolateral extension of the parabrachial nucleus, and the results of water and NaCl intake with injections in the KF nucleus were not different from those with injections in the central lateral and dorsolateral portions of the LPBN. As estimated from the injection of methylene blue, the spread of the injection was confined in most rats above the superior cerebellar peduncle (SCP). In a few animals there was spread of the injection into the SCP but never below this structure.
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From a total of 77 rats used in this study, 52 had histologically confirmed bilateral LPBN injections as described above.
Effects of LPBN Proglumide Injections on 0.3 M NaCl and Water Intake When Given in Conjunction With Intracerebroventricular ANG II and When Given Alone (Protocols 1, 4, and 6)
Presented in Fig. 2 are the intakes of 0.3 M NaCl and water in response to intracerebroventricular ANG II when either vehicle or proglumide (50 µg · 200 nl1 · site1)
was administered in random order into the LPBN
(protocol
1). Bilateral LPBN proglumide (50 µg · 200 nl1 · site1)
pretreatment significantly increased 0.3 M NaCl intake induced by
intracerebroventricular ANG II
[F(1,14) = 5.83;
P < 0.05] (Fig. 2). The water
intake to intracerebroventricular ANG II after LPBN proglumide (50 µg · 200 nl1 · site1)
pretreatment when NaCl was simultaneously available was not significantly different than that under the LPBN vehicle condition (i.e., no main effect of treatment). However, there was a significant treatment × time interaction
[F(3,42) = 4.42;
P < 0.05] (Fig. 2). Also
plotted in Fig. 2 are the NaCl solution and water intakes for a subset
of animals tested with a smaller dose of proglumide (10 µg · 200 nl1 · site1)
injected into the LPBN. The smaller dose of proglumide (10 µg · 200 nl1 · site1)
qualitatively appeared to have an enhancing effect on 0.3 M NaCl intake
that was smaller than the 50 µg/200 nl dose. (The 10 µg · 200 nl1 · site1
treatment was not part of the randomized experimental design and
therefore the data were not statistically tested.)
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With only water available (protocol
4), proglumide (10 µg · 200 nl1 · site1)
pretreatment produced no significant change in
intracerebroventricular ANG II-induced intake
[F(1,13) = 1.19;
P > 0.05] (Fig.
3). (The data for the 50 µg · 200 nl1 · site1
pretreatment dose are also plotted in Fig. 3 but were not statistically tested.)
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Bilateral injection of proglumide (50 µg · 200 nl1 · site1)
into the LPBN in the absence of a dipsogenic-natriorexigenic treatment produced virtually no 0.3 M NaCl (0.5 ± 0.2 ml) or water intake over 120 min after injection (0.2 ± 0.2 ml)
(protocol
6, n = 7 rats).
Effects of LPBN Proglumide Injections on 0.3 M NaCl and Water Intake Induced by Combined Treatment With Furo + Cap (Protocol 2)
Bilateral LPBN injections of proglumide (50 µg · 200 nl1 · site1)
produced marked increases in both 0.3 M NaCl
[F(1,8) = 10.25; P < 0.05] and water intake
[F(1,8) = 21.91;
P < 0.05] induced by combined
subcutaneous treatment with Furo + Cap (Fig.
4).
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Effects of LPBN CCK-8 Injections on 0.3 M NaCl and Water Intake Induced by Combined Treatment With Furo + Cap (Protocol 3)
Bilateral injections of CCK-8 (0.5 µg · 200 nl1 · site1)
into the LPBN produced no overall change in 0.3 M NaCl intake
[F(1,5) = 1.63;
P > 0.05] but reduced water
intake [F(1,5) = 14.75;
P < 0.05] induced by the
treatment with Furo + Cap (Fig. 5).
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Effect of CCK-8 Injections Into the LPBN on Intracerebroventricular ANG II-Induced Water Intake (Protocol 5)
Pretreatment with bilateral injections of CCK-8 (0.1 µg · 200 nl1 · site1)
into the LPBN significantly reduced water intake induced by intracerebroventricular ANG II
[F(1,7) = 11.78;
P < 0.05] (Fig. 6).
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DISCUSSION |
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Top
Abstract
Introduction
Materials & Methods
Results
Discussion
References
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The correction of extracellular hypovolemia requires the ingestion of not only water but also of solute, such as ionic sodium, which does not readily cross the cell plasma membrane and remains in the extracellular space. Both thirst and salt appetite-related behaviors promote the expansion of extracellular fluid volume. The present results viewed in this light indicate that bilateral administration of the nonselective CCK receptor antagonist proglumide into the LPBN enhances behavior associated with restoring or expanding extracellular fluid volume. The effect was most evident in the marked increases of hypertonic NaCl intake induced by intracerebroventricular administration of ANG II and during a hypovolemic hypotensive state (29) after combined administration of Furo + Cap. The LPBN proglumide-associated 3- to 10-fold increases in salt intake to the natriorexigenic-dipsogenic treatments (i.e., Furo + Cap and intracerebroventricular ANG II, respectively) suggest that intake of hypertonic saline is under some type of tonic LPBN-CCK-associated inhibitory control. In this light, it is particularly noteworthy that, in the absence of hypovolemia/hypotension or of intracerebroventricular ANG II, bilateral LPBN administration of proglumide did not stimulate salt appetite in and of itself.
The effects of proglumide on water intake were less pronounced than the effects on salt intake. That is, with the two experimental manipulations used to induce intake, approximately a twofold increase in water drinking in response to proglumide treatment was seen with the Furo + Cap treatment and about a 40% increase was observed in conjunction with intracerebroventricular ANG II. The smaller increases in water intake in comparison to NaCl consumption after proglumide treatment in conjunction with the dipsogenic-natriorexigenic treatments do not appear to be the result of inducing a competing behavior (i.e., the animals directing their consumption to the NaCl solution). When animals were given access to only water, LPBN proglumide did not increase water intake induced by intracerebroventricular ANG II. Although water intake was significantly increased after administration of Furo + Cap, it is possible that the water intake was secondary to cellular (osmotic) dehydration produced by the large amount of 0.3 NaCl consumed. Further investigation will be necessary to determine whether the enhanced water intake after bilateral LPBN proglumide injections associated with Furo + Cap treatment is a primary or secondary effect.
To determine if the enhancing effects of proglumide on NaCl and water intake were in fact related to an action on CCK receptors, the effects of bilateral LPBN CCK-8 administration were studied in animals given the Furo + Cap and the intracerebroventricular ANG II treatments. In the first case, both 0.3 M NaCl and water were available, whereas in the latter, only water was present. In the case of the intracerebroventricular ANG II challenge, only water was presented to the animal because typically the intake of hypertonic NaCl induced by intracerebroventricular ANG II is fairly modest (e.g., ~1 ml/60 min; see Fig. 2) and therefore essentially precludes observing a suppression of such a small NaCl intake. In both the Furo + Cap and intracerebroventricular ANG II tests, bilateral LPBN administration of CCK-8 suppressed the behaviors associated with expansion of extracellular volume. In the Furo + Cap test, the suppression of water intake was constant throughout the test, whereas the reduction of 0.3 M NaCl ingestion was most apparent early in the test period. Again these results are consistent with the interpretation that CCK action in the LPBN is to suppress behaviors that expand extracellular fluid volume.
The present results showing marked NaCl intake after the blockade of CCK receptors in the LPBN are another indication of the importance of central inhibitory mechanisms in the control of NaCl intake. Such central inhibitory mechanisms have been shown to also involve 5-HT, oxytocin, and tachykinins (2, 6, 16, 18, 26, 27). Studies involving central manipulations of 5-HT, oxytocin, and now CCK indicate that blockade of inhibitory mechanisms strongly facilitates NaCl intake in the presence of excitatory stimuli (e.g., ANG II). However, a functional blockade of an inhibitory mechanism by itself does not appear to be sufficient to induce reliable NaCl intake. For example, injection of proglumide into the LPBN in the absence of another treatment (i.e., intracerebroventricular ANG II or subcutaneous Furo + Cap) produced no change in NaCl or water intake.
The present study along with previous work investigating the LPBN (6, 17, 18) suggests that at least two different neurotransmitters (5-HT and CCK) acting in this structure may have an inhibitory role in the control of NaCl and water intake. 5-HT and CCK also inhibit food intake, and a model of cooperativity and interdependence between the two neurochemicals has been proposed by Cooper and Dourish (8) in the inhibitory control of feeding. These investigators suggest that in response to food ingestion, both endogenous 5-HT and CCK are released. The cooperativity assumption is that elevated 5-HT tends to increase CCK release and actions and vice versa. The interdependence assumption is that both 5-HT and CCK act at their respective receptors for the normal development of satiety. Pharmacological interventions that block either 5-HT or CCK receptors reduce the satiety-inducing effects of either transmitter. One assumption of this idea is that elevated 5-HT and CCK activity is necessary for satiation to be fully expressed. Blocking either component will consequently affect the capacity of the other component to induce a satiety effect. In addition, it is also suggested that elevated 5-HT tends to promote CCK activity and vice versa, so that there is a form of mutual cooperativity. With this model, it is clear that receptor antagonists acting at either 5-HT or CCK receptors also functionally antagonize responses mediated by the companion receptor system. Future studies will be necessary to show whether the model developed for the control of food intake by Cooper and Dourish (8) also applies for the effects of 5-HT and CCK injections into the LPBN and the inhibition of NaCl and water intake.
Accumulating evidence indicates that the LPBN is a major site within a central neural network related to the control of cardiovascular regulation and of body fluid homeostasis. The LPBN projects to several forebrain areas involved in the control of water and electrolyte balance (central nucleus of the amygdala, paraventricular nucleus of the hypothalamus, bed nucleus of the stria terminalis, median preoptic nucleus) and also receives afferent inputs from multiple regions (5, 9, 13, 15, 24) also implicated in fluid homeostasis. One important input to the LPBN arises from AP/mNTS. Ablation and chemical stimulation studies have implicated both the AP/mNTS and the LPBN in the control of NaCl and water intake (6, 7, 17, 18, 20, 21). In the rat, the brain circuitry related to the action of CCK on feeding involves both the hindbrain (AP, NTS, parabrachial nucleus) and forebrain (ventromedial hypothalamus and paraventricular hypothalamic nucleus). Peripheral sensory input is conveyed by the vagus to the NTS (4, 19). From the NTS, information may be conveyed either directly to the supraoptic, paraventricular, and ventromedial nuclei of the hypothalamus or indirectly to the hypothalamus by way of the parabrachial nucleus (5, 9, 12, 13, 15, 24). It is possible that CCK may act as a neurotransmitter/neuromodulator at each step of this projection.
Studies also suggest that central oxytocin inhibits NaCl intake (2). Peripheral administration of CCK activates oxytocin neurons in the supraoptic and paraventricular hypothalamic nuclei and increases oxytocin secretion (23). It is reasonable to consider the possibility that changes in NaCl intake after injection of CCK agonist and antagonist into the LPBN could be due to changes in central oxytocin release.
Studies showing that decreases in arterial pressure facilitate NaCl intake after the treatment with Furo + Cap (29) and that inflation of a right atrial balloon inhibits fluid intake (30) suggest that signals arising from systemic baroreceptors can modulate water and NaCl intake. Because electrolytic lesions of the LPBN abolish the inhibition of water intake observed during the inflation of a right atrial balloon, it has been proposed that input from cardiopulmonary baroreceptors is processed in the LPBN (21). The precise nature of the stimuli that signal the brain of volume expansion is not clear, but the effects of atrial stretch may be due to the activation of neural and/or humoral mechanisms. Neural afferents from arterial and cardiopulmonary baroreceptors reach the AP/mNTS (4). On the other hand, humoral mechanisms may involve the release of atrial natriuretic peptide (ANP) by atrial distention. It has been shown that central or peripheral administration of ANP reduces dipsogenic responses (1). The AP is a brain area rich in ANP receptors. Because the AP lacks a blood-brain barrier, plasma ANP may initially activate this area and this information is then carried to the LPBN. The AP/mNTS also receives information from the stomach and other parts of the digestive system by way of the vagus, and CCK is suggested to be a neurotransmitter signal for satiety in this pathway (10).
Perspectives
These results reinforce the idea of the importance of hindbrain inhibitory mechanisms in the control of water and NaCl intake and demonstrate that more studies on inhibitory mechanisms are necessary for a clearer understanding of thirst and salt appetite. Future studies need to determine 1) if 5-HT and CCK in the LPBN interact in the control of water and NaCl intake and 2) the types of peripheral signals that activate CCKergic and serotonergic mechanisms in the LPBN.| |
ACKNOWLEDGEMENTS |
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We thank Terry G. Beltz for expert technical assistance and Andrea Zardetto-Smith for photomicrograph preparation.
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FOOTNOTES |
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This research was supported by grants from the National Heart, Lung, and Blood Institute (HL-14388 and HL 57472), from the National Aeronautics and Space Administration (NAG5-6171), from the Office of Naval Research (N00014-97-1-0145), and Fundação de Amparo à Pesquisa do Estado de São Paulo (Proc. 93/0167-7).
Address for reprint requests: A. K. Johnson, Dept. of Psychology, Univ. of Iowa, 11 Seashore Hall E, Iowa City, IA 52242-1407.
Received 7 November 1996; accepted in final form 6 July 1998.
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Top
Abstract
Introduction
Materials & Methods
Results
Discussion
References
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