Arginine vasopressin, fever and temperature regulation

Pittman, Quentin J.; Chen, Xihua; Mouihate, Abdeslam; Hirasawa, Michiru; Martin, Sheilagh

doi:10.1016/s0079-6123(08)61582-4

Cited by 63 publications

(42 citation statements)

References 79 publications

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“…As the brain is thought to have its own antipyretic system, attention focused on the existence of a possible endogenous antipyretic as the cause of this suppression. A likely candidate was AVP, for which there is persuasive evidence that it acts as an endogenous antipyretic (39). Initial evidence in support of AVP acting to suppress fever at term came from the observation that there is increased immunoreactivity for AVP in the hypothalamus during pregnancy in guinea pigs (27) and in push-pull perfusates of the preoptic area in rats (19).…”

Section: Discussionmentioning

confidence: 99%

Suppression of fever at near term is associated with reduced COX-2 protein expression in rat hypothalamus

Mouihate¹,

Ms²,

Nakamura

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

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Suppression of fever at near term is associated with reduced COX-2 protein expression in rat hypothalamus. Am J Physiol Regul Integr Comp Physiol 283: R800-R805, 2002; 10.1152/ ajpregu.00258.2002The fever response is blunted at near term. As the enzyme cyclooxygenase-2 (COX-2) plays a critical role in fever development, we measured its expression in rat hypothalamus during pregnancy and lactation. Western blot analysis revealed a 72-kDa COX-2-immunoreactive band in non-immune-challenged, pregnant rats at day 15 of pregnancy. In contrast, it was almost undetectable at near term and at lactation day 5. COX-2 was significantly induced at the 15th day of pregnancy and at the 5th lactating day after intraperitoneal lipopolysaccharide (50 g/kg). However, this COX-2 induction was significantly reduced at near term compared with values before and after term. The protein levels of the EP3 receptor in the hypothalamus, one of the prostaglandin E 2 (PGE2) receptors suggested to be a key receptor for fever induction, were unaffected throughout the pregnancy and lactation in both non-immune-challenged and lipopolysaccharide-treated rats. These data suggest that suppression of fever at near term is associated with a significantly reduced induction of COX-2 by lipopolysaccharide, resulting in a reduced production of PGE 2. Altered expression of the EP3 receptor does not seem to be involved in this fever refractoriness at near term.cyclooxygenase-2; parturition; lipopolysaccharide; prostaglandin receptor; EP3 receptor FEVER, A MAJOR PART of host defense, is thought to be of beneficial and adaptive value (15). Thus the inability to develop a fever response to pathogens can be detrimental (16). An absent or reduced fever has been observed in pregnant animals at near term (14) and, in some circumstances, is associated with abortion or mortality (23). This febrile refractoriness has been observed in many species, including guinea pig (55), rabbits (28), sheep (14), and rats (7,23,24), and has been observed in response to both peripherally injected pyrogens (14, 23, 55) and, to a lesser extent, to centrally infused prostaglandins (7,24,48). The fact that fever suppression is most dramatic in response to systemically administered LPS suggests that several steps in the cascade of responses to peripherally injected LPS may be affected.In response to bacterial pyrogens such as LPS, immunocompetent cells generate endogenous cytokines, which signal to the central nervous system through either humoral or neuronal pathways (for review, see Ref. 8) to induce expression of cyclooxygenase-2 (COX-2) (6, 22). The activity of this enzyme results in the cyclooxygenation of arachidonic acid and subsequently the production of PGE 2 , which acts largely in the anterior hypothalamus/preoptic area (47). COX-2 is present in basal conditions in the brain (3, 41), but in inflammation, it is induced specifically in the endothelium of brain capillaries (18,25). Levels of COX-2 have been correlated to levels of PGE 2 during LPS-induced fever (54). Because...

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Section: Discussionmentioning

confidence: 99%

Suppression of fever at near term is associated with reduced COX-2 protein expression in rat hypothalamus

Mouihate¹,

Ms²,

Nakamura

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

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“…This is of particular interest because vasopressin functions as an antipyretic peptide (Naylor et al, 1988;Pittman and Wilkinson, 1992;Pittman et al, 1998). Pittman and colleagues found that injection or infusion of exogenous vasopressin into ventral septal area or central medial amygdala reduces fever in most mammals (Cooper et al, 1979a,b;Federico et al, 1992).…”

Section: Potential Functional Implications Of V 1 Agonist-induced Supmentioning

confidence: 99%

Suppression of Proinflammatory Cytokines Interleukin-1β and Tumor Necrosis Factor-α in Astrocytes by a V₁Vasopressin Receptor Agonist: A cAMP Response Element-Binding Protein-Dependent Mechanism

Zhao¹,

Brinton²

2004

J. Neurosci.

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“…8, 20, and 39). The same hormones are involved in febrile pathogenesis, most (melanocortins, glucocorticoids, arginine vasopressin) as antipyretics (40,46,70) but some (angiotensin II) as fever promoters (73). Therefore, lesions of the OVLT and its surrounding structures may affect febrile responsiveness by interfering with the complex balance of anti-and propyretic substances and not exclusively by modifying febrigenic signaling processes.…”

Section: Hyperthermia Induced By Ovlt Lesionmentioning

confidence: 99%

The organum vasculosum laminae terminalis in immune-to-brain febrigenic signaling: a reappraisal of lesion experiments

Romanovsky

Sugimoto²,

Simons³

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

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Romanovsky, Andrej A., Naotoshi Sugimoto, Christopher T. Simons, and William S. Hunter. The organum vasculosum laminae terminalis in immune-to-brain febrigenic signaling: a reappraisal of lesion experiments. Am J Physiol Regul Integr Comp Physiol 285: R420-R428, 2003. First published April 24, 2003 10.1152/ajpregu.00757. 2002The organum vasculosum laminae terminalis (OVLT) has been proposed to serve as the interface for blood-to-brain febrigenic signaling, because ablation of this structure affects the febrile response. However, lesioning the OVLT causes many "side effects" not fully accounted for in the fever literature. By placing OVLT-lesioned rats on intensive rehydration therapy, we attempted to prevent these side effects and to evaluate the febrile response in their absence. After the OVLT of Sprague-Dawley rats was lesioned electrolytically, the rats were given access to 5% sucrose for 1 wk to stimulate drinking. Sucrose consumption and body mass were monitored. The animals were examined twice a day for signs of dehydration and treated with isotonic saline (50 ml/kg sc) when indicated. This protocol eliminated mortality but not several acute and chronic side effects stemming from the lesion. The acute effects included adipsia and gross (14% of body weight) emaciation; chronic effects included hypernatremia, hyperosmolality, a suppressed drinking response to hypertonic saline, and previously unrecognized marked (by ϳ2°C) and long-lasting (Ͼ3 wk) hyperthermia. Because the hyperthermia was not accompanied by tail skin vasoconstriction, it likely reflected increased thermogenesis. After the rats recovered from the acute (but not chronic) side effects, their febrile response to IL-1␤ (500 ng/kg iv) was tested. The shamoperated rats developed typical monophasic fevers (ϳ0.5°C), the lesioned rats did not. However, the absence of the febrile response in the OVLT-lesioned rats likely resulted from the untreatable side effects. For example, hyperthermia at the time of pyrogen injection was high enough (39-40°C) to solely prevent fever from developing. Hence, the changed febrile responsiveness of OVLT-lesioned animals is given an alternative interpretation, unrelated to febrigenic signaling to the brain. fever; adipsia; third ventricle; median preoptic nucleus THERE IS LITTLE DOUBT that the febrile response is regulated by the central nervous system (CNS), but the mechanisms by which peripherally originating pyrogenic signals reach the brain remain unclear. At least four possibilities have been proposed. First, pyrogenic cytokines, such as IL-1␤, access the CNS by carriermediated transport across the blood-brain barrier (BBB) (2). Second, circulating pyrogens bind to the cerebral vascular endothelium and stimulate production of fever mediators, most importantly PGE 2 , by endothelial cells; endotheliocytes release PGE 2 into the brain tissue (10). Third, pyrogens act on neural terminals in peripheral tissues and convey febrigenic signals to the CNS via sensory fibers, e.g., those of the vagus nerve (7, 74). Fourt...

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Arginine vasopressin, fever and temperature regulation

Cited by 63 publications

References 79 publications

Suppression of fever at near term is associated with reduced COX-2 protein expression in rat hypothalamus

Suppression of fever at near term is associated with reduced COX-2 protein expression in rat hypothalamus

Suppression of Proinflammatory Cytokines Interleukin-1β and Tumor Necrosis Factor-α in Astrocytes by a V₁Vasopressin Receptor Agonist: A cAMP Response Element-Binding Protein-Dependent Mechanism

The organum vasculosum laminae terminalis in immune-to-brain febrigenic signaling: a reappraisal of lesion experiments

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Arginine vasopressin, fever and temperature regulation

Cited by 63 publications

References 79 publications

Suppression of fever at near term is associated with reduced COX-2 protein expression in rat hypothalamus

Suppression of fever at near term is associated with reduced COX-2 protein expression in rat hypothalamus

Suppression of Proinflammatory Cytokines Interleukin-1β and Tumor Necrosis Factor-α in Astrocytes by a V1Vasopressin Receptor Agonist: A cAMP Response Element-Binding Protein-Dependent Mechanism

The organum vasculosum laminae terminalis in immune-to-brain febrigenic signaling: a reappraisal of lesion experiments

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Suppression of Proinflammatory Cytokines Interleukin-1β and Tumor Necrosis Factor-α in Astrocytes by a V₁Vasopressin Receptor Agonist: A cAMP Response Element-Binding Protein-Dependent Mechanism