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1 Faculdade de Odontologia de Ribeirão Preto, 2 Escola de Enfermagem de Ribeirão Preto, and 3 Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, 14040-904 Ribeirão Preto, São Paulo, Brazil
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ABSTRACT |
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Top
Abstract
Introduction
Materials & Methods
Results
Discussion
References
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It has been reported that arginine
vasopressin (AVP) plays a thermoregulatory action, but very little is
known about the mechanisms involved. In the present study, we tested
the hypothesis that nitric oxide (NO) plays a role in systemic
AVP-induced hypothermia. Rectal temperature was measured before and
after AVP, AVP blocker, or
NG-nitro-L-arginine methyl ester
(L-NAME; NO synthase inhibitor) injection. Control animals received saline injections of the same volume. The basal body temperature
(Tb) measured in control animals was 36.53 ± 0.08°C. We observed a significant
(P < 0.05) reduction in
Tb to 35.44 ± 0.19°C after
intravenous injection of AVP (2 µg/kg) and to 35.74 ± 0.10°C
after intravenous injection of
L-NAME (30 mg/kg). The systemic
injection of the AVP blocker
[
-mercapto-,-cyclopentamethylenepropionyl1,O-Et-Tyr2,Val4,Arg8]vasopressin
(10 µg/kg) caused a significant increase in
Tb to 37.33 ± 0.23°C,
indicating that AVP plays a tonic role by reducing Tb. When the treatments with AVP
and L-NAME were combined,
systemically injected L-NAME
blunted AVP-induced hypothermia. To assess the role of central
thermoregulatory mechanisms, a smaller dose of L-NAME (1 mg/kg) was injected
into the third cerebral ventricle. Intracerebroventricular injection of
L-NAME caused an increase in
Tb, but when
intracerebroventricular L-NAME
was combined with systemic AVP injection (2 µg/kg), no change in
Tb was observed. The data indicate
that central NO plays a major role mediating systemic AVP-induced
hypothermia.
endothelium-derived relaxing factor; temperature; nitric oxide synthase; arginine vasopressin
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INTRODUCTION |
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Top
Abstract
Introduction
Materials & Methods
Results
Discussion
References
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NITRIC OXIDE (NO), a diffusible lipophilic gas, has been recognized as a physiologically relevant molecule for playing a role not only in blood pressure control (26) but also in water balance (13) and body temperature (Tb) regulation (5, 29). The family of NO synthases (NOS), the enzymes that produce NO in vivo, consists of two different classes, i.e., the inducible and constitutive forms (20). NOS proteins and their mRNAs have been identified in the neural circuitry for regulation of body fluid homeostasis (14, 36), including arginine vasopressin (AVP) secretion (13).
It is well known that AVP plays an important role in the regulation of arterial blood pressure (8, 31) and plasma osmolarity (9). More recently, it has been shown that the central AVP is one of the main endogenous antipyretic molecules (6). In addition, intracerebroventricular administration of AVP is known to elicit hypothermia (15, 17, 23). These observations show that AVP plays an important role in thermoregulation in the central nervous system (CNS).
In contrast, as far as we are concerned, there is only one published study of the systemic effect of AVP (30) in which a reduction of Tb was measured after the peptide was administered peripherally. This effect was largely attributed to the baroreflexive suppression of nonshivering thermogenesis, i.e., a reduction of interscapular brown adipose tissue thermogenesis. The firing rate of sympathetic nerves innervating brown adipose tissue (10) as well as brown fat blood flow (21) are decreased by peripheral NOS inhibitors. Conversely, the NO pathway in the CNS seems to be activated to produce hypothermia (5).
In the present study, we tested the hypothesis that NO plays a role in the systemic effect of AVP on Tb of normothermic rats.
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MATERIALS AND METHODS |
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Top
Abstract
Introduction
Materials & Methods
Results
Discussion
References
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Animals. Experiments were performed on adult male Wistar rats weighing 200-260 g, housed at controlled temperature (25 ± 2°C) and exposed to a daily 12:12-h light-dark cycle. The animals were allowed free access to water and food. Experiments were performed between 10:00 AM and 3:00 PM.
Surgery. Animals were anesthetized with tribromoethanol (Aldrich, Milwaukee, WI) and implanted with a Silastic catheter through the external jugular vein into the right atrium according to the technique of Arms and Ojeda (1). After surgery, animals were treated with 100,000 U of benzylpenicillin and allowed to recover for 4 days before experimentation. During this period, the catheters were flushed daily with heparinized saline.
Rats used for intracerebroventricular administration were also anesthetized with tribromoethanol and fixed in a stereotaxic frame. A stainless steel guide cannula (0.7 mm OD) was introduced into the third cerebral ventricle (coordinates: A
0.4 mm, L 0 mm, D
7.8-8.5 mm) (25). 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. The surgical procedures were
performed over a period of 40 min. Experiments were initiated 1 wk
after cannula placement.
Determination of temporal effect of AVP injection on Tb. Rats previously cannulated in the jugular vein were housed in a plastic chamber (5 liters) for at least 2 h before control Tb was measured by inserting a thermoprobe into the colon each time Tb was to be measured. It should be pointed out that, before the experiment, the animals were habituated to temperature measurements which were performed quickly to avoid any stress-induced elevations in Tb. The animals were then treated with AVP (Peninsula Laboratories) dissolved in pyrogen-free sterile saline by intravenous bolus injection of 0.4, 2, and 10 µg/kg body wt and Tb was measured 10, 20, and 30 min after injection. The volume of each injection was 0.2 ml, and the drug was flushed in with 0.3 ml of heparinized saline. Control animals received intravenous injections of saline (0.5 ml).
Determination of effect of an AVP blocker on
Tb.
Control Tb was determined after an
initial 2-h period, and rats were treated with
[-mercapto-,-cyclopentamethylenepropionyl1,O-Et-Tyr2,Val4,Arg8]vasopressin
(Sigma, St. Louis, MO) dissolved in saline, a vasopressor antagonist of
AVP with low antidiuretic antagonist activity, by intraperitoneal
injection of 4, 10, and 40 µg/kg body wt 1 h before the
Tb measurements. Doses, method of
administration, and period of time after injection when
Tb was determined were chosen on the basis of previous studies (18, 19, 28). Control animals were
treated with intraperitoneal injection of saline.
Determination of effect of a NOS blocker on Tb. The same animal chamber was used for all experiments. After the animals habituated to the experimental condition (~2 h), control Tb was measured, and experimental rats were then treated with NG-nitro-L-arginine methyl ester (L-NAME, Sigma) dissolved in saline by intravenous bolus injection of 1, 10, 30, and 60 mg/kg body wt 1 h before the measurements. This period of time was chosen on the basis of previous studies that assessed the effect of L-NAME on Tb (5, 29). The volume of each injection was 0.2 ml, and the drug was flushed in with 0.3 ml of heparinized saline. Control animals received intravenous injections of saline.
Determination of combined effects of exogenous AVP and L-NAME on Tb. Control Tb was determined after an initial 2-h period, and L-NAME was injected intravenously (30 and 60 mg/kg) or intracerebroventricularly (1 mg/kg) 1 h before AVP injection. This period of time was chosen on the basis of previous studies (5, 29). AVP was then injected intravenously (2 µg/kg), and Tb was measured 10 min later. Control animals were injected with the same volume of saline.
In the rats that received an intracerebroventricular injection of L-NAME (1 mg/kg), a 10-µl Hamilton syringe and a dental injection needle (Missy, 200 µm OD) were used for intracerebroventricular injections, and L-NAME was dissolved in a final volume of 1 µl. Injection was performed over a period of 2 min, and to avoid reflux, 1 min was allowed to elapse before the injection needle was removed from the guide cannula.Statistical analysis. All values in this study are reported as means ± SD. Changes in Tb were evaluated by ANOVA or ANOVA for repeated measures to analyze the temporal effect of exogenous AVP on Tb. The difference between means was assessed by the Tukey-Kramer multiple comparisons test. Values of P < 0.05 were considered to be significant.
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RESULTS |
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Top
Abstract
Introduction
Materials & Methods
Results
Discussion
References
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In all experimental protocols, Tb ranged from 36.1 to 37.0°C during the control period, and baseline values of the experimental groups did not differ significantly from the saline group. During the experiments, mean chamber temperature was 25.4 ± 0.8°C, and room temperature was 24.6 ± 0.9°C.
Effect of exogenous AVP on Tb. Figure 1 shows the effect of AVP intravenous injection on Tb. When animals were treated with AVP (2 and 10 µg/kg), a significant decrease in Tb was observed, whereas saline or AVP at the dose of 0.4 µg/kg caused no significant change. The dose of 2 µg/kg produced a significant drop in Tb 10 and 20 min after injection, whereas 10 µg/kg reduced Tb until the end of the experiment. The dose of 2 µg/kg was chosen for further experiments, and the effect of systemic AVP on Tb was determined 10 min after injection.
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Effect of intraperitoneal injection of AVP blocker on Tb. Figure 2 shows that intraperitoneal injection of an AVP blocker at the doses of 10 and 40 µg/kg produced a significant increase (P < 0.05) in Tb, whereas the dose of 4 µg/kg did not produce significant changes.
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Effect of the NOS blocker on Tb. When 30 mg/kg of L-NAME was injected intravenously, Tb decreased from 36.52 ± 0.13 to 35.74 ± 0.10°C. When a higher dose (60 mg/kg) was applied, no change was observed. Saline or L-NAME at the doses of 1 and 10 mg/kg caused no significant change in Tb. These data are plotted in Fig. 3.
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Combined effects of exogenous AVP and intravenous injection of
L-NAME on
Tb.
Figure 4 shows the effect of AVP on
Tb after saline or
L-NAME injection, given as the
difference between Tb before and
after AVP injection (
Tb). The
reduction in Tb after AVP
injection was significantly smaller (P < 0.05) in animals treated with
L-NAME at the dose of 60 mg/kg
compared with animals treated with saline. Treatment with
L-NAME at the dose of 30 mg/kg
did not significantly reduce the magnitude of the drop in
Tb after AVP injection
(Tb) compared with saline.
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Combined effects of exogenous AVP and intracerebroventricular injection of L-NAME on Tb. Intracerebroventricular injection of 1 mg/kg L-NAME caused a significant increase (P < 0.05) in Tb from 36.57 ± 0.09 to 36.93 ± 0.22°C, whereas saline injection had no effect. The combination of intracerebroventricular saline injection and AVP (2 µg/kg) intravenous injection caused a significant drop in Tb (P < 0.01), similar to that obtained by application of AVP only. However, AVP failed to induce a reduction in Tb when L-NAME was given intracerebroventricularly; i.e., there was no significant difference between the intracerebroventricular L-NAME and intracerebroventricular L-NAME plus intravenous AVP groups. These data are plotted in Fig. 5.
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DISCUSSION |
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Top
Abstract
Introduction
Materials & Methods
Results
Discussion
References
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The present study provides evidence that the NO pathway in the CNS participates in AVP-induced hypothermia because intracerebroventricular injection of a NOS blocker (L-NAME) altered the reduction in Tb induced by AVP (Fig. 5). In addition, we report that AVP plays a tonic role by reducing Tb because an increase in Tb was observed after treatment with an AVP antagonist (Fig. 2).
A previous study (30) has shown that [Lys8]vasopressin peripheral injection in rats causes a drop in Tb, which is greatly reduced after bilateral sinoaortic deafferentation. The authors concluded that the effect of systemic vasopressin can be attributed, at least in part, to the baroreflexive suppression of nonshivering thermogenesis. Additionally, peripheral AVP also can alter Tb by interacting with the CNS through receptors present in the vessels of the circumventricular organs of the brain (cf. Refs. 11, 35), since AVP has very low permeability across the blood-brain barrier (24). Naylor et al. (23) found that central injection of AVP into a lateral ventricle cause hypothermia, whereas AVP injected into the preoptic area produced hyperthermia, with no effect on blood pressure in either case (30). Our data add the participation of the NO pathway in the CNS for the effect of systemic AVP, which may act via baroreceptors and/or circumventricular organs.
A secondary mechanism that can promote an alteration in Tb is ventilation. AVP might alter ventilation by increasing arterial pressure. It was reported that an increase in arterial pressure can cause hypoventilation through stimulation of the aortic and carotid sinus baroreceptors (cf. Ref. 33), a fact that may reduce the ventilatory heat loss, promoting an increase in Tb. It was also reported that AVP does not alter ventilation in rats (35). This fact shows that ventilation does not play a role in the thermoregulatory actions induced by systemic AVP.
Previous studies have reported that the AVP
V1-receptor blockers,
[-mercapto-,-cyclopentamethylenepropionyl1,O-Me-Tyr2,Arg8]vasopressin
and 1-desamino-8-D-arginine
vasopressin injected into the CNS, do not affect
Tb (7, 16, 22). Conversely, our
data show that the AVP V1-receptor
blocker
[-mercapto-,-cyclopentamethylenepropionyl1,O-Et-Tyr2,Val4,Arg8]vasopressin,
when injected systemically, causes an increase in Tb. Most likely, this difference
might be due to the effect of the blocker on AVP receptors located at
different sites. Although the AVP receptor blocker used in the present
study shows a higher affinity for
V1 than for
V2 receptors (18, 19), Sawyer et al. (28) observed that this same blocker, injected intraperitoneally, also acts on AVP V2-receptors at
least at the doses of 10 and 30 µg/kg. Therefore the present study
provides evidence that AVP plays a tonic role in thermoregulation, but
it is uncertain by which receptor.
A number of recent studies have shown that NO accounts for a large part of the biological actions of endothelium-derived relaxing factor (20). The importance of NO can be demonstrated by inhibition of the effects of NO (27) by using L-arginine analogs, such as L-NAME. In the present study, we have chosen L-NAME because it is a nonselective inhibitor of NOS and acts on both the constitutive and inducible isoforms of the enzymes.
The dose-effect curve shown in Fig. 3 was "U" shaped. The exact reason for this shape is not known; however, we suggest that it may be due to the multiple sites of action of L-NAME. These sites seem to be distributed throughout the body, including the CNS, where they are responsible for neural mechanisms that increase Tb (5). Nevertheless, L-NAME intravenous injection at the dose of 30 mg/kg caused a significant reduction in Tb despite the fact that L-NAME should decrease cutaneous heat loss, since it causes vasocontriction of both large and small arteries (4, 27, 32). Probably, L-NAME at the dose of 30 mg/kg elicits hypothermia by reducing the firing rate of sympathetic nerves innervating interscapular brown adipose tissue (10) as well as brown fat blood flow (21). However, when a higher dose of L-NAME (60 mg/kg) was applied, no change in Tb was observed. It has previously been shown that an intravenous L-NAME injection of 30 mg/kg markedly decreases not only endothelial but also neural NO production (27, 34). Moreover, Iadecola et al. (12) reported that intravenous administration of L-NAME to rats leads to a partial inhibition, i.e., no more than ~50% inhibition of brain NOS catalytic activity, in a dose- and time-dependent manner. In these experiments, the doses of L-NAME were between 5 and 40 mg/kg, and the NOS activity was determined 30 min after injection. Probably, L-NAME injection at the dose of 60 mg/kg produced a stronger inhibition of NOS activity in the CNS, activating neural mechanisms to increase Tb (5). It seems clear, then, that the role of NO in Tb is complex and varies according to drug concentration.
Treatment of the rats with L-NAME alters AVP-induced hypothermia in a dose-dependent manner (Fig. 4). When L-NAME at the dose of 60 mg/kg was applied, a significant reduction in the magnitude of the AVP-induced hypothermia was observed. This might be due to the fact that L-NAME at the dose of 60 mg/kg reduces ~50% of NO production in the CNS (12, 34). Corroborating this hypothesis is our finding that intracerebroventricular injection of a small amount of L-NAME (1 mg/kg) prevented the AVP-induced hypothermia (Fig. 5). It was recently reported that intracerebroventricular injection of L-NAME at the dose of 1 mg/kg completely abolished brain NOS activity 90 min after injection (2).
In conclusion, our data indicate that the NO pathway in the CNS acts as a physiological messenger molecule mediating systemic AVP-induced hypothermia (Fig. 6). In addition, endogenous AVP seems to play a tonic role in thermoregulation.
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Perspectives
We have shown that the NO pathway in the CNS plays a major role in AVP-induced hypothermia. The central NO pathway may be a common mediator for many hypothermic stimuli, such as hypoxia (5), hypercapnia (3), and AVP (present study). Furthermore, central NOS inhibition, per se, causes an increase in Tb (5, 10). Further studies using NOS antagonists or antisense oligonucleotides to NOS injections at specific sites of the CNS are needed to firmly establish the mechanisms underlying the role NO in rat thermoregulation. Although the exact mechanisms remain to be determined, central NO clearly plays an important role in thermoregulation by mediating hypothermic stimuli.| |
ACKNOWLEDGEMENTS |
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We acknowledge the excellent technical assistance of Mauro F. Silva.
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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, and Pronex. A. A. Steiner was the recipient of a FAPESP undergraduate scholarship.
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. §1734 solely to indicate this fact.
Address for reprint requests: L. G. S. Branco, Dept. de Fisiologia, Faculdade de Odontologia de Ribeirão Preto/USP, 14040-904 Ribeirão Preto, São Paulo, Brazil.
Received 3 February 1998; accepted in final form 2 June 1998.
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 F. M. Paro, M. C. Almeida, E. C. Carnio, and L. G. S. Branco Role of L-glutamate in systemic AVP-induced hypothermia J Appl Physiol, January 1, 2003; 94(1): 271 - 277. [Abstract] [Full Text] [PDF]
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S. Subramanian, B. Erokwu, F. Han, T. E. Dick, and K. P. Strohl L-NAME differentially alters ventilatory behavior in Sprague-Dawley and Brown Norway rats J Appl Physiol, September 1, 2002; 93(3): 984 - 989. [Abstract] [Full Text] [PDF]
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A. A. Steiner and L. G. S. Branco Carbon monoxide is the heme oxygenase product with a pyretic action: evidence for a cGMP signaling pathway Am J Physiol Regulatory Integrative Comp Physiol, February 1, 2001; 280(2): R448 - R457. [Abstract] [Full Text] [PDF]
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A. A. Steiner, E. C. Carnio, and L. G. S. Branco Role of neuronal nitric oxide synthase in hypoxia-induced anapyrexia in rats J Appl Physiol, September 1, 2000; 89(3): 1131 - 1136. [Abstract] [Full Text] [PDF]
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L. G. S. Branco, A. A. Steiner, G. J. Tattersall, and S. C. Wood Role of adenosine in the hypoxia-induced hypothermia of toads Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2000; 279(1): R196 - R201. [Abstract] [Full Text] [PDF]
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K. C. Bicego-Nahas, A. A. Steiner, E. C. Carnio, J. Antunes-Rodrigues, and L. G. S. Branco Antipyretic effect of arginine vasotocin in toads Am J Physiol Regulatory Integrative Comp Physiol, June 1, 2000; 278(6): R1408 - R1414. [Abstract] [Full Text] [PDF]
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A. A. Steiner, E. Colombari, and L. G. S. Branco Carbon monoxide as a novel mediator of the febrile response in the central nervous system Am J Physiol Regulatory Integrative Comp Physiol, August 1, 1999; 277(2): R499 - R507. [Abstract] [Full Text] [PDF]
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