Endogenous antipyretics: neuropeptides and glucocorticoids

Roth, Joachim; Zeisberger, Eugen; Vybíral, S; Janský, L

doi:10.2741/1277

Cited by 49 publications

(23 citation statements)

References 93 publications

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“…Although the mechanisms underlying the regulated hypothermia observed during sepsis are not fully understood, it is likely to result from the interaction of pyrogenic and antipyretic agents. AVP is believed to be an endogenous antipyretic agent [4,12,13,32] . An elevation in plasma AVP levels has been associated with a more intense period of hypothermia during endotoxemia [33] .…”

Section: Discussionmentioning

confidence: 99%

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Thermoregulation and Vasopressin Secretion during Polymicrobial Sepsis

Oliveira-Pelegrin

Ravanelli²,

Branco³

et al. 2008

Neuroimmunomodulation

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Objective: We investigated the time course of thermoregulation, nitric oxide (NO) formation and hydroelectrolytic alterations, as well as mean arterial pressure and arginine vasopressin (AVP) secretion, in experimental sepsis induced by cecal ligation and puncture (CLP). Methods: Male Wistar rats submitted to CLP or a sham operation were divided into 4 groups, as follows: group 1, for survival rate evaluation for 24 h; group 2, for body temperature (Tb) analysis; group 3, for mean arterial pressure registration, and group 4, for blood collection and processing of the neurohypophysis and hypothalamic nuclei 0, 2, 4, 6 and 24 h after surgery. AVP levels and content were measured in plasma, neurohypophysis and the hypothalamic paraventricular and supraoptic nuclei. Results: Animals which underwent CLP showed high mortality, a progressive decrease in mean arterial pressure and an increase in plasma NO. Tb dropped during the first 4 h and showed a progressive increase 6 h after surgery. Plasma AVP levels increased immediately after CLP surgery and again at 6 h, before returning to basal levels at 24 h. This was followed by a depletion of neurohypophyseal AVP content at 4 h that continued until 24 h. AVP content in the supraoptic nucleus was elevated 24 h after CLP surgery, while in the paraventricular nucleus, an increase was observed at 6 h and 24 h. Conclusions: In the present study, laparotomy and hypotension may have been responsible for the increase in plasma AVP in the initial phase of polymicrobial sepsis, and this may have contributed to the observed hypothermia. Moreover, an apparently impaired replenishment of AVP content in the neurohypophysis, possibly due to increased NO formation, may explain the impaired AVP secretion in the late phase of severe sepsis.

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Section: Discussionmentioning

confidence: 99%

“…A considerable amount of data indicate that a number of endogenously produced factors have antipyretic properties in vivo. These include factors such as melanocyte-stimulating hormone, glucocorticoids, TNF-␣ , angiotensin II, cholecystokinin and arginine vasopressin (AVP) [5,[11][12][13] .…”

Section: Introductionmentioning

confidence: 99%

Thermoregulation and Vasopressin Secretion during Polymicrobial Sepsis

Oliveira-Pelegrin

Ravanelli²,

Branco³

et al. 2008

Neuroimmunomodulation

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“…Accordingly to our data, the benefi cial effect of the glucocorticoids may be functionally associated with prevention of lowering of body temperature. The maintenance of temperature homeostasis by glucocorticoid hormones (Roth et al, 2004) could be a fundamental of their benefi cial action on the gastric mucosa during cold-restraint stress.…”

Section: Glucocorticoids Released During Hpa Axis Activation Protect mentioning

confidence: 99%

Hypothalamic-pituitary-adrenocortical axis: the hidden gold in gastric mucosal homeostasis

et al. 2006

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The results overviewed in the present article suggest that glucocorticoids released during acute activation of hypothalamic-pituitary-adrenocortical (HPA) axis are important gastroprotective factors, allowing us to re-evaluate the traditional point of view about their ulcerogenic role. It has been shown that various ulcerogenic stimuli induce an increase in glucocorticoid production that in turn helps the gastric mucosa to resist against a harmful action of ulcerogenic stimuli. Glucocorticoids released in response to mild stress contribute to adaptive gastric cytoprotection. The gastroprotective action of glucocorticoids is accounted for by maintaining the local defensive factors and inhibiting the pathogenic elements. Maintenance of glucose and temperature homeostasis as well as systemic blood pressure by glucocorticoid hormones could be a fundamental of their beneficial action on various gastric targets. Thus, glucocorticoids released during activation of HPA axis may contribute to the gastric mucosal homeostasis through their contribution to general body homeostasis.

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“…Below we will discuss the neural pathways and mediators of fever and anapyrexia in connection with roles of NO, CO, and H 2 S in these responses. For other mechanistic aspects of these responses, we refer the reader to a collection of reviews by other investigators (31,88,125,148,170,178,196,197,216,229,278,281,286,288,300,332,334,354,393).…”

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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Endogenous antipyretics: neuropeptides and glucocorticoids

Cited by 49 publications

References 93 publications

Thermoregulation and Vasopressin Secretion during Polymicrobial Sepsis

Thermoregulation and Vasopressin Secretion during Polymicrobial Sepsis

Hypothalamic-pituitary-adrenocortical axis: the hidden gold in gastric mucosal homeostasis

Gaseous Mediators in Temperature Regulation

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