Inducible nitric oxide synthase pathway in the central nervous system and vasopressin release during experimental septic shock*

Giusti‐Paiva, Alexandre; Castro, Margaret de; Antunes‐Rodrigues, José; Cárnio, Evelin C.

doi:10.1097/00003246-200206000-00025

Cited by 85 publications

(82 citation statements)

References 25 publications

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“…Vasopressin was administered, however, also for a second reason. Thus, in the early phase of septic shock a reflex increase in vasopressin is found (Tarpey et al, 1998;Landry & Oliver, 2001;Giusti-Paiva et al, 2002), which, however, cannot occur in pithed animals since reflex loops involving the brain are destroyed. The possibility that vasopressin acted via a presynaptic site had to be considered.…”

Section: G Godlewski Et Almentioning

confidence: 99%

Presynaptic cannabinoid CB₁ receptors are involved in the inhibition of the neurogenic vasopressor response during septic shock in pithed rats

Godlewski

Malinowska

Schlicker

2004

British J Pharmacology

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1 Our study was undertaken to investigate whether bacterial endotoxin/lipopolysaccharide (LPS) affects the neurogenic vasopressor response in rats in vivo by presynaptic mechanisms and, if so, to characterize the type of presynaptic receptor(s) operating in the initial phase of septic shock. ). The four antagonists by themselves did not affect the increase in DBP induced by ES or by injection of NA in rats not exposed to LPS. 4 We conclude that in the initial phase of septic shock, the activation of presynaptic CB 1 receptors by endogenously formed cannabinoids contributes to the inhibition of the neurogenic vasopressor response.

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Section: G Godlewski Et Almentioning

confidence: 99%

Presynaptic cannabinoid CB₁ receptors are involved in the inhibition of the neurogenic vasopressor response during septic shock in pithed rats

Godlewski

Malinowska

Schlicker

2004

British J Pharmacology

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“…Hence, we will refer to this response as anapyrexia. Of interest is the fact that LPS-induced anapyrexia usually occurs alongside with hypotensive shock (4,13,63,114,189,200,262,285), an observation that raises the question as to whether hypoxia associated with LPS shock is the trigger of the fever-anapyrexia switch. This question has not yet been answered, though a study involving cyclooxygenase inhibition points to a possible disconnect between the anapyrexic and hypotensive responses to a high LPS dose (338).…”

Section: Regulated Changes In T B : Fever and Anapyrexiamentioning

confidence: 99%

Gaseous Mediators in Temperature Regulation

Branco

Soriano

Steiner

2014

Comprehensive Physiology

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Deep body temperature (Tb) is kept relatively constant despite a wide range of ambient temperature variation. Nevertheless, in particular situations it is beneficial to decrease or to increase Tb in a regulated manner. Under hypoxia for instance a regulated drop in Tb (anapyrexia) is key to reduce oxygen demand of tissues when oxygen availability is diminished, leading to an increased survival rate in a number of species when experiencing low levels of inspired oxygen. On the other hand, a regulated rise in Tb (fever) assists the healing process. These regulated changes in Tb are mediated by the brain, where afferent signals converge and the most important regions for the control of Tb are found. The brain (particularly some hypothalamic structures located in the preoptic area) modulates efferent activities that cause changes in heat production (modulating brown adipose tissue activity and perfusion, for instance) and heat loss (modulating tail skin vasculature blood flow, for instance). This review highlights key advances about the role of the gaseous neuromodulators nitric oxide (NO), carbon monoxide (CO), and hydrogen sulfide (H2S) in thermoregulation, acting both on the brain and the periphery.

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“…Following these procedures, rats were immediately decapitated for collection of blood. The doses of LPS and L-NAME and the time interval between the drugs were chosen on the basis of previous studies [2,8,32] and because pilot experiments indicated that this protocol lead to the most consistent and repeatable results.…”

Section: Experimental Protocolsmentioning

confidence: 99%

“…Moreover, it has been demonstrated that NO mediates physiological responses in the central nervous system (CNS), immune system and endocrine system [13]. It has also been demonstrated that NO may act as a modulator of vasopressin (AVP) release/synthesis in normal [18,35] and septic rats [8]. AVP plays an important role in the regulation of arterial blood pressure and osmolarity.…”

Section: Introductionmentioning

confidence: 99%

Role of nitric oxide in thermoregulation during septic shock: involvement of vasopressin

Giusti‐Paiva

Branco

Castro

et al. 2003

Pflugers Arch - Eur J Physiol

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We tested the hypothesis that the nitric oxide (NO) pathway in the central nervous system (CNS) plays a role in hypothermia, as well as in the febrile response during experimental septic shock, by regulating vasopressin (AVP) release. Experiments were performed on male Wistar rats treated with NG-nitro-L-arginine methyl ester (L-NAME), a non-selective NO synthase (NOS) inhibitor, injected intracerebroventricularly (250 microg/1 microl) 30 min before lipopolysaccharide (LPS) 1.5 mg/kg i.v. injection. One hour after LPS administration we observed a significant drop in body temperature (hypothermic response), followed by a temperature increase after the second hour (febrile response), which remained until the end of the experiment. Increased plasmatic AVP levels were concomitantly observed during hypothermia, nearly returning to basal levels during the febrile phase. When L-NAME was administered with LPS, plasmatic AVP concentrations remained high throughout the experiment, hypothermia was accentuated and the febrile response was abolished. Additionally, pre-treatment with beta-mercapto-beta,beta-cyclopentamethylenepropionyl1, O-Et-Tyr2, Val4, Arg8-vasopressin, an AVP V1 receptor blocker (10 microg/kg) administered i.v., reduced hypothermia and exacerbated the febrile response to endotoxin. In conclusion, our data indicate that the central NO pathway plays an inhibitory role in AVP release during experimental septic shock, which seems to be critical for the thermoregulation during this pathophysiological state.

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Inducible nitric oxide synthase pathway in the central nervous system and vasopressin release during experimental septic shock*

Abstract: These data indicate that central nitric oxide arising from the inducible nitric oxide synthase pathway plays an important inhibitory role in vasopressin release during experimental septic shock and may be responsible for the hypotension occurring in this vasodilatory shock.

Cited by 85 publications

References 25 publications

Presynaptic cannabinoid CB₁ receptors are involved in the inhibition of the neurogenic vasopressor response during septic shock in pithed rats

Presynaptic cannabinoid CB₁ receptors are involved in the inhibition of the neurogenic vasopressor response during septic shock in pithed rats

Gaseous Mediators in Temperature Regulation

Role of nitric oxide in thermoregulation during septic shock: involvement of vasopressin

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Inducible nitric oxide synthase pathway in the central nervous system and vasopressin release during experimental septic shock*

Abstract: These data indicate that central nitric oxide arising from the inducible nitric oxide synthase pathway plays an important inhibitory role in vasopressin release during experimental septic shock and may be responsible for the hypotension occurring in this vasodilatory shock.

Cited by 85 publications

References 25 publications

Presynaptic cannabinoid CB1 receptors are involved in the inhibition of the neurogenic vasopressor response during septic shock in pithed rats

Presynaptic cannabinoid CB1 receptors are involved in the inhibition of the neurogenic vasopressor response during septic shock in pithed rats

Gaseous Mediators in Temperature Regulation

Role of nitric oxide in thermoregulation during septic shock: involvement of vasopressin

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Presynaptic cannabinoid CB₁ receptors are involved in the inhibition of the neurogenic vasopressor response during septic shock in pithed rats

Presynaptic cannabinoid CB₁ receptors are involved in the inhibition of the neurogenic vasopressor response during septic shock in pithed rats