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1 Faculdade de Medicina de Ribeirão Preto, 2 Escola de Enfermagem de Ribeirão Preto, and 3 Faculdade de Odontologia de Ribeirão Preto, Universidade de São Paulo, 14040-904 Ribeirão Preto, Brazil
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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It has been reported that
systemic injection of arginine vasopressin (AVP) induces a drop in body
core temperature (Tc), but little is known about the
mechanisms involved. Because glutamate is an important excitatory
neurotransmitter involved in a number of thermoregulatory actions, in
the present study, we tested the hypothesis that glutamate plays a role
in systemic AVP-induced hypothermia. Wistar rats were pretreated
intracerebroventricularly (icv) with kynurenic acid, an antagonist of
L-glutamate ionotropic receptors,
-methyl-(4-carboxyphenyl)glycine (MCPG), an antagonist of
L-glutamate metabotropic receptors, or saline 15 min before intravenous injection of AVP (2 µg/kg) or saline. Tc,
brown adipose tissue (BAT) temperature, blood pressure, heart rate, and
tail skin temperature were measured continuously. Administration of saline icv followed by intravenous AVP caused a significant drop in
Tc brought about by a reduction in BAT thermogenesis and an increase in heat loss through the tail. MCPG treatment (icv) did not
affect the fall in Tc induced by AVP. Treatment with
kynurenic acid (icv) abolished AVP-induced hypothermia but did not
affect the AVP-evoked rise in blood pressure or drop in heart rate and BAT temperature. Heat loss through the tail was significantly reduced
in animals injected with AVP and pretrated with kynurenic acid. These
data indicate that ionotropic receptors of L-glutamate in
the central nervous system participate in peripheral AVP-induced hypothermia by affecting heat loss through the tail.
temperature; arginine vasopressin; ionotropic glutamate receptors; metabotropic glutamate receptors
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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IT IS WELL KNOWN THAT the peptide arginine vasopressin (AVP) plays an important role in the regulation of arterial blood pressure (BP) (7, 34) and osmolarity (7). More recently, it has been shown that AVP plays an important role in thermoregulation, because it is one of the main endogenous antipyretic molecules in the central nervous system (CNS) (5). Moreover, intravenous (iv) AVP administration produces an immediate fall in body core temperature (Tc) in rats (15, 23). Few studies have assessed the mechanism by which AVP evokes the drop in Tc when it is administered peripherally. Shido et al. (31) attributed this effect to the baroreflexive suppression of nonshivering termogenesis, i.e., a reduction of interscapular brown adipose tissue (BAT) thermogenesis; however, heat loss through the tail was not assessed. Modulation of BAT thermogenesis had already been reported for other vasopressor substances like norepinephrine, phenylephrine (12, 30), and angiotensin II (10), which indicates that the effect of AVP, at least the hypothermic one, may not be selective. In the present study, we have chosen AVP as an experimental model to induce hypothermia because a number of previous studies used AVP (15, 23, 31, 33), which allows one to easily reconcile the available data. Furthermore, catecholamines, per se, have a thermoregulatory function since they can directly induce BAT thermogenesis (11).
To our knowledge, only one study by our laboratory
(33) has assessed the central mechanism involved in
AVP-induced hypothermia, showing that the neuromodulator nitric oxide
plays an important role in AVP-induced hypothermia.
L-Glutamate is another key excitatory neurotransmitter that
has been shown to participate in thermoregulation (3, 13)
and baroreflex function (4). Glutamate receptors are
divided into two major classes: ionotropic glutamate receptors and
metabotropic glutamate receptors. Ionotropic glutamate receptors are
ligand-gated ion channels. They can be classified into three types
named for their most selective agonists:
N-methyl-D-aspartate (NMDA), kainic acid, and
DL--amino-3-hydroxy-5-methylisoxazole-propionic acid.
All of these ionotropic glutamate receptor types are antagonized by
kynurenic acid (2). In contrast to the ionotropic
glutamate receptors, the metabotropic glutamate receptors are G
protein-coupled receptors that modulate second messenger systems. The
metabotropic glutamate receptors can be antagonized by
-methyl-(4-carboxyphenyl)glycine (MCPG) (6).
In the present study, we tested the hypothesis that L-glutamate plays a role in AVP-induced hypothermia. To this end, we used kynurenic acid and MCPG and measured Tc, BAT temperature (TBAT), BP, heart rate (HR), and heat loss through the tail. Our data indicate that L-glutamate ionotropic receptors are involved in AVP-induced hypothermia increasing heat loss through the tail but play no role in baroreflex-mediated suppression of nonshivering thermogenesis.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Animals. Experiments were performed on adult male Wistar rats weighing 220-320 g, housed at controlled temperature (23 ± 1°C), and exposed to a daily 12:12-h light-dark cycle. Animals were allowed free access to water and food. Experiments started at 9:00 AM. Animal care was provided in compliance with the guidelines set by the American Physiological Society (1).
Surgery.
Rats were anesthetized with 2,2,2-tribromoethanol and fixed in a
stereotaxic frame. A stainless steel guide cannula (0.7 mm outer
diameter) was introduced into the third cerebral ventricle (coordinates: A = 
0.4 mm, L = 0 mm,
D = 7.8-8.5mm from the skull surface)
(24). The displacement of the meniscus in a water
manometer ensured correct positioning of the cannula in the third
ventricle. The cannula was attached to the bone with stainless steel
screws and acrylic cement. A tight-fitting stylet was kept inside the guide cannula to prevent occlusion. Animals were then implanted with a
silastic catheter through the external jugular vein into the right
atrium, according to the technique of Harms and Ojeda (9).
In animals used for Tc and heat loss index (HLI)
measurements, a biotelemetry transmitter (model ER-4000,
Mini-Mitter, Sunriver, OR) was implanted intraperitoneally. Animals
that were submitted to TBAT measurements were implanted
with a biotelemetry transmitter positioned under BAT (31).
After surgery, animals were treated with 1,200,000 U of pentabiotic and
allowed to recover for 5 days before experimentation. During this
period, the catheters were flushed daily with 25 U of heparinized
saline. Surgical procedures were performed over a period of 40 min.
Drugs. AVP was purchased from Peninsula Laboratories. Kynurenic acid and MCPG were purchased from Sigma Chemical. These drugs were dissolved in pyrogen-free sterile saline.
Tc measurements. Tc was measured by biotelemetry (Mini-Mitter) at 2-min intervals and plotted at 4-min intervals over a period of 30 min before and 90 min after the treatments. Data were acquired and fed to an IBM computer by using the Vital View software (Mini-Mitter). Rats were left undisturbed in individual cages for at least 24 h before the experiment. Before each treatment, initial Tc was determined as the average of the last five Tc measurements made at 2-min intervals.
TBAT measurements. TBAT was measured by biotelemetry at 2-min intervals and plotted at 4-min intervals over a period of 30 min before and 90 min after the treatments. Rats were left undisturbed for at least 24 h before the experiment. Before each treatment, initial TBAT (TBATi) was determined as the average of the last five TBAT measurements made at 2-min interval.
HLI.
To evaluate HLI through the tail skin, the tail skin temperature was
measured with a thermistor (type YSI 402, Cole Parmer Instrument)
attached to the ventral surface of the tail at the border of its
proximal and middle thirds. Measurements were made every 4 min
simultaneously with Tc recordings by biotelemetry. Tail
skin temperature values were then compared with ambient temperature and
Tc and were expressed as HLI according to the formula
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BP and HR measurements. BP was measured by means of the arterial catheter with a pressure transducer for a period of 15 min before and 90 min after the treatments. Data were acquired and fed to an IBM computer using the Poly View software. HR was determined by counting pressure pulses.
Experimental protocols. A 705-LT, 10-µl Hamilton syringe and a dental injection needle (200 µm outer diameter; Mizzy) were used for intracerebroventricular (icv) injections. Injection was performed over a period of 1 min, and 1 min was allowed to elapse before the injection needle was removed from the guide cannula to avoid reflux.
For the determination of the effect of kynurenic acid on AVP-induced hypothermia, rats were icv treated with saline (2 µl) or kynurenic acid (100 nmol/2 µl) and 15 min later received AVP by an iv bolus injection of 2 µg/kg body wt. The kynurenic acid dose was chosen on the basis of pilot experiments and a previous study (35), whereas the AVP dose was chosen on the basis of a previous study from our laboratory (33). The volume of each iv injection was 0.2 ml, and the drug was flushed in with 0.3 ml of saline. Control animals received iv injections of saline (0.5 ml). Another group of animals received an iv injection of kynurenic acid at the same dose as was used intracerebroventricularly to test whether the effect of kynurenic acid on AVP-induced hypothermia was indeed confined to the CNS. To evaluate the effect of MCPG on AVP-induced hypothermia, rats received an icv injection of saline (4 µl) or MCPG (100, 200, or 500 nmol/4 µl), followed 15 min later by an iv injection of AVP (2 µg/kg). Control animals received iv injections of saline (0.5 ml). MCPG doses were chosen on the basis of previous studies (8). Basal BP and HR were determined during a period of 15 min. Rats were then icv treated with saline (2 µl) or kynurenic acid (100 nmol/2 µl) and after 15 min received an iv injection of AVP (2 µg/kg). Control animals received iv injections of saline (0.5 ml). To determine the effect of kynurenic acid and AVP on BAT thermogenesis, TBAT was measured in animals icv injected with kynurenic acid or saline followed by an iv injection of AVP or saline. To determine the effect of kynurenic acid and AVP on HLI, rats received an icv injection of kynurenic acid or saline followed by an iv injection of AVP or saline, and tail skin temperature was measured concomitantly with Tc. HLI was then calculated.Statistical analysis. All values in this study are reported as means ± SE. Values of Tc and TBAT are the changes from basal values. Data were analysed statistically by two-way ANOVA followed by Student's t-test to assess differences between groups. Values of P < 0.05 were considered to be significantly different.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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In all experimental protocols, Tc ranged from 36.9 to 37.8°C during the control period. No difference in initial Tc or TBATi values was observed among the different groups. Initial Tc and TBATi values are shown in the figures. During the experiments, room temperature was kept at 23 ± 0.5°C.
Figure 1, A and C,
shows the effect of icv injection of saline,
kynurenic acid (100 nmol/2 µl), or MCPG (100, 200, or 500 nmol/4
µl) combined with iv injection of saline on Tc. Animals icv injected with kynurenic acid, MCPG, or saline showed no significant change in Tc. Figure 1B shows the effect of
kynurenic acid on AVP-induced hypothermia. A Tc reduction
of 0.9 ± 0.3°C was observed after icv treatment with saline
followed by iv injection of AVP. Treatment with kynurenic acid icv
abolished AVP-induced hypothermia (P < 0.05). Figure 1D shows the effect of MCPG
treatment on AVP-induced hypothermia. MCPG did not affect the fall in
Tc induced by AVP irrespectively of the dose used.
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Figure 2 shows the effect of iv injection
of kynurenic acid at the same dose as injected icv. Injection of saline
or kynurenic acid iv combined with iv injection of AVP caused a drop of
0.7 ± 0.2 and 0.8 ± 0.2°C in Tc, respectively
(P > 0.05), with no significant difference between
these values.
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TBATi ranged from 37.3 to 37.9°C during the control
period. Animals icv injected with saline or kynurenic acid combined
with iv injection of saline showed no significant changes in
TBAT. When animals were icv injected with saline or
kynurenic acid and iv injected with AVP, a TBAT reduction
of 0.7 ± 0.1 and 0.7 ± 0.2°C, respectively, was observed
(P > 0.05). No significant differences were observed
among rats icv injected with saline or kynurenic acid followed by iv
injection of AVP. These data are shown in Fig.
3.
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Basal BP and HR ranged from 93 to 107 mmHg and from 354 to 389 beats/min, respectively. Injection of saline or kynurenic acid icv
caused no significant change in BP or HR when combined with iv saline
injection (Fig. 4A). When
animals received an icv injection of saline followed by an iv injection
of AVP, BP increased from 102 ± 2.4 to 149 ± 2 mmHg
(P < 0.05) and HR decreased from 389 ± 16 to
178 ± 10 beats/min (P < 0.05). The rise in BP
and the drop in HR were not affected by icv treatment with kynurenic
acid. These data are depicted in Fig. 4B.
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HLI was not affected in animals icv injected with kynurenic acid or saline and iv injected with saline. In animals that received an icv injection of saline combined with an iv injection of AVP, HLI increased from 0.5 ± 0.1 to 0.8 ± 0.1. Kynurenic acid completely abolished the increase in HLI induced by AVP. In animals that received an icv injection of kynurenic acid combined with an iv injection of AVP, basal HLI was 0.6 ± 0.1, and no change in HLI was observed after AVP injection.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The present study provides evidence that central L-glutamate ionotropic receptors play a role in systemic AVP-induced hypothermia, since icv pretreatment with kynurenic acid, an antagonist of glutamate ionotropic receptors, abolished the drop in Tc induced by iv injection of AVP. Moreover, we showed that hypothermia induced by AVP is brought about by a coordinated response of reduced thermogenesis in BAT and increased heat loss through the tail. Additionally we showed that kynurenic acid did not affect TBAT, BP, and HR responses to AVP, indicating that its action is not via baroreflexive suppression of nonshivering thermogenesis. On the other hand, we provided evidence that kynurenic acid abolishes AVP-induced hypothermia inhibiting heat loss through the tail, since pretreatment with kynurenic acid abolished the increase in HLI induced by AVP. Furthermore, it seems that central L-glutamate metabotropic receptors blocked by MCPG play no role in AVP-induced hypothermia, since icv pretreatment with MCPG, an L-glutamate metabotropic receptor antagonist, did not affect hypothermia elicited by AVP.
Previous studies have reported that AVP plays an important role in thermoregulation. AVP is one of the main endogenous antipyretic molecules in the CNS (5). Moreover, icv administration of AVP may elicit hypothermia (16, 18, 22), and intrapreoptic administration of AVP induces grooming, which is known to increase heat loss and thus plays a role in thermoregulation (19).
Besides central effects, iv or intraperitoneal injection of AVP produces an immediate decrease in Tc (15, 23). However, little is known about the mechanism of AVP-induced hypothermia in rats. Itoh (15) has shown that hypothermia induced by iv injection of AVP is not abolished by anterior hypothalamic lesion, and he concluded that vasopressin injected peripherally did not act on the hypothalamic thermoregulatory center.
It has been reported that administration of vasopressor substances such
as norephinephrine and phenylephrine suppresses heat production through
the sinoaortic baroreceptor reflex in unanesthethized animals
(12, 29, 30, 36). In 1984, Shido et al. (31) demonstrated that the fall in Tc after peripheral injection
of AVP is greatly reduced after bilateral sinoaortic deafferentation. The authors concluded that the effect of systemic AVP on Tc
could be attributed, at least in part, to the baroreflexive suppression of nonshivering thermogenesis. Because BAT is under sympathetic nervous
system control (11, 28), the lowered metabolism after vasopressin may be due to reduced sympathetic nervous activity in the
tissue (30). On the other hand, Morrison (20)
suggested that sympathetic activity to BAT is under weak baroreflex
control. One may argue that under thermoneutral conditions there is
little spontaneous activity in BAT sympathetic nerves. However, it is important to note here that the thermoneutral zone of rats is about
28°C, and because our experiments were performed at ~23°C, our
rats presumably had an increased spontaneous sympathetic activity in
BAT, a response that agrees with the present observation that iv
injection of AVP caused a reduction in TBAT. Interestingly, in the present study, icv kynurenic acid abolished AVP-induced hypothermia without affecting the reduced TBAT and reflex
bradicardia, indicating that the baroreflexive suppression of
nonshivering thermogenesis to BAT is not under central glutamatergic
control. Additionally, heat loss through the tail seems to be the
mechanism involved in AVP-induced hypothermia modulated by central
L-glutamate (Fig. 5).
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In the rat, ~20% of total body heat loss occurs by sympathetically mediated increases in blood flow through an elaborate system of arteriovenous anastomoses in the skin of its tail (32, 38). It is important to note that the skin is known to be innervated by two distinct branches of the sympathetic nervous system: an adrenergic vasoconstrictor system that contributes to resting cutaneous vascular tone and a cholinergic vasodilator system featuring an unknown neurotransmitter coreleased with acetylcholine (17). In this study, we showed that kynurenic acid abolished AVP-induced hypothermia by reducing heat loss through the tail (Fig. 5). It is interesting to note that AVP evokes a drop in Tc by a coordinated process that includes not only a reduction in TBAT but also an increase in heat loss through the tail. Interestingly, kynurenic acid abolished HLI but not TBAT responses to AVP, suggesting that different structures may be involved in the control of thermogenesis and heat loss. Accordingly, it has been well established that effector mechanisms responsible for the control of Tc are dissociated. The specific nuclei in the CNS involved in the action of L-glutamate on peripheral AVP-induced hypothermia in rats are not known and will require further research. The preoptic area of the hypothalamus is an important thermosensitive site (14). Efferent pathways from the preoptic region descend to different regions involved in the control of skin blood flow and thus are implicated in the control of Tc. In rats, the raphe nuclei seem to be crucial structures to the control of skin vasomotion and thus to the control of Tc (21). Interestingly, L-glutamate injection into the raphe activated tail sympathetic nerve (25).
Internal Tc results from a steady state determined by the heat production (shivering and nonshivering thermogenesis) and heat loss (evaporative and nonevaporative heat loss) balance (27). Although kynurenic acid completely blocked the AVP-induced hypothermia, it had no effect on the AVP-induced decrease of TBAT. Thus we speculate that some unknown compensatory mechanism may exist.
The metabotropic glutamate receptors have been assigned to three distinct groups (26). Group 1 consists of metabotropic glutamate receptors subtypes 1 and 5. Group 2 comprises subtypes 2 and 3. Group 3 members consist of subtypes 4, 6, 7, and 8. Groups 1 and 2 can be antagonized by MCPG (6). For group 3 receptors, no metabotropic glutamate receptor subtype 4 antagonists have been found, subtype 6 is exclusively retinal, and little data are available regarding metabotropic glutamate receptors subtype 8 (26). In the present study, rats icv injected with MCPG showed no significant changes in Tc, which indicates that metabotropic glutamate receptors, at least the subtypes that are blocked by MCPG, in the CNS do not play a tonic role in the maintenance of the Tc of euthermic animals under the experimental conditions used in the present study. Furthermore, icv pretreatment with MCPG caused no change in the course of the fall in Tc induced by AVP, suggesting that central metabotropic glutamate receptors play no role in AVP-induced hypothermia. It is important to emphasize that the MCPG dose used in the present study is about 2.5-fold higher than the maximal dose frequently used to block metabotropic glutamate receptors (8), indicating that these receptors are unlikely to be involved in these responses.
L-Glutamate has been shown to participate in a number of different pathological and physiological conditions. Figure 1B shows that icv pretreatment with kynurenic acid abolished AVP-induced hypothermia, indicating that ionotropic glutamate receptors participate in this response. Interestingly, ionotropic glutamate receptors have been shown to participate in pyrogenic fever (13) as well as in hypothermia induced by dithiothreitol (3). In agreement, several studies favor the involvement of NMDA receptors in thermoregulatory function. Pechnick et al. (24a) observed a rise in Tc after acute inhibition of NMDA receptors by (±)-dizocilpine maleate (MK 801), a glutamate NMDA antagonist. On the other hand, in situ injections of L-glutamate into the dorsomedial hypothalamus reduce the thermogenic activity, whereas injections into the medial preoptic area lead to a biphasic response with a decrease followed by an increase in heat production (37).
In summary, in addition to the baroreflex-mediated suppression of nonshivering thermogenesis (31), the present data indicate that L-glutamate modulates AVP-induced hypothermia in the rat CNS by acting via ionotropic receptors and affecting blood flow and consequently heat loss through the tail.
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ACKNOWLEDGEMENTS |
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We thank Mauro F. Silva, Nadir Martins Fernandes, and Daniela Lima de Oliveira for excellent technical assistance.
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FOOTNOTES |
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This work was supported by Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP), Conselho Nacional de Desenvolvimento Científico e Tecnológico, Programa de Apoio a Núcleos de Excelência, and Fundação de Apoio ao Ensino, Pesquisa e Assistência do Hospital das clínicas da Faculdade de Medicina de Ribeirão Preto-Universidade de São Paulo. F. M. Paro and M. C. Almeida are the recipients of FAPESP and Coordenação de aperfeiçoamento de pessoal de nível superior graduate scholarships, respectively.
Address for reprint requests and other correspondence: L. G. S. Branco, Departamento de Morfologia, Estomatologia e Fisiologia, Faculdade de Odontologia de Ribeirão Preto, USP, 14040-904 Ribeirão Preto, SP, Brazil (E-mail: branco{at}forp.usp.br).
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.
October 4, 2002;10.1152/japplphysiol.00291.2002
Received 5 April 2002; accepted in final form 26 September 2002.
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RESULTS
DISCUSSION
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