The contribution of epinephrine to experimentally induced urethral inflammation in the rat

Nordling, L.; Lundeberg, Thomas; Liedberg, H.; Theodorsson, Elvar; Ekman, Peter

doi:10.1016/0304-3940(92)90544-h

Cited by 12 publications

(4 citation statements)

References 9 publications

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“…Proinflammatory properties of epinephrine, reversible by ␤-receptor blockade or adrenal medullectomy, have been suggested by other in vivo models of inflammation (21)(22)(23)(24). However, both immunosuppressive and immunostimulatory effects of catecholamines have been described (25), with several recent in vitro studies suggesting that catecholamines suppress the release of proinflammatory cytokines (26)(27).…”

Section: Discussionmentioning

confidence: 99%

Corticotropin-releasing hormone deficiency unmasks the proinflammatory effect of epinephrine

Karalis

Kontopoulos

Muglia

et al. 1999

Proc. Natl. Acad. Sci. U.S.A.

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Traditionally, the adrenal gland has been considered an important endocrine component of the pathway to inhibit acute inflammation via hypothalamic corticotropin-releasing hormone (CRH)-mediated secretion of glucocorticoid. Immunoreactive CRH found in inflamed tissues is a potent proinflammatory factor. Using genetic and pharmacological models of CRH deficiency, we now show that CRH deficiency unmasks a major proinflammatory effect of epinephrine secreted from the adrenal medulla. Together, epinephrine and peripheral CRH stimulate inflammation, and glucocorticoid acts as a counterbalancing force in this regard. Our findings suggest that stimulation of the acute inflammatory response should be included with the other “fight-or-flight” actions of epinephrine.

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Section: Discussionmentioning

confidence: 99%

Corticotropin-releasing hormone deficiency unmasks the proinflammatory effect of epinephrine

Karalis

Kontopoulos

Muglia

et al. 1999

Proc. Natl. Acad. Sci. U.S.A.

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“…This effect is reversed with repeated treatment of adrenaline and salbutamol. Conversely, high-dosage adrenaline decreased experimentally induced urethral inflammation (Nordling et al, 1992). In addition to these studies, a previous study suggests that adrenal gland hormones play an important role in the antiinflammatory effects of tamoxifen by decreasing the Fig.…”

Section: Resultsmentioning

confidence: 94%

Effects of paracetamol and etodolac on plasma adrenaline levels of rats

2014

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Adrenaline, which is released from the adrenal medulla, is an important compound in the reaction of sympathetic nerve system. This hormone can increase the body's normal metabolic rate up to 100 %, and thus improves the effectiveness of the whole body. It has been considered to be involved in the control of inflammation. Therefore, we investigated whether there are effects of paracetamol and etodolac on adrenaline levels of rats after oral administration. The rats were divided into three subgroups while analysing the effects of adrenaline on paracetamol and etodolac. The first group was the control, second group was composed of rats given paracetamol, and third group was composed of rats given etodolac. In order to measure adrenaline plasma concentration, we have used the high-performance liquid chromatography coupled with fluorescence detection. According to the result of the analysis, there are statistically important differences at adrenaline levels between control group and rats-applied drugs. Obtained results showed that although adrenaline level in the paracetamol-applied group decreased, adrenaline level in the etodolac-applied group increased. It is concluded that different effects of etodolac and paracetamol on circulating adrenaline levels can be related to their different effects on inflammation, COX enzymes, prostaglandins, etc. Also we can suggest usage of paracetamol instead of etodolac in patients with cardiovascular system diseases.

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“…The data we have presented indicate that the stress‐induced effect on plasma extravasation in both male and female rats is dependent on an intact sympathoadrenal axis. Although it has previously been shown that adrenal medulla‐derived epinephrine enhances inflammation in female rats (Nordling et al ., 1992), it is unlikely that epinephrine is the sole mediator of the effect of sound stress as, when given alone, continuously administered stress levels of epinephrine did not affect the magnitude of bradykinin‐induced plasma extravasation. However, coadministration of stress levels of epinephrine and corticosterone resulted in a suppression of bradykinin‐induced plasma extravasation in males and an enhancement in females, i.e.…”

Section: Discussionmentioning

confidence: 99%

Sexual dimorphism in the effect of nonhabituating stress on neurogenic plasma extravasation

Green

Levine

2005

Eur J of Neuroscience

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The sympathoadrenal axis contributes to the sexual dimorphism of the inflammatory response. As stress both activates the sympathoadrenal axis and profoundly affects inflammation and inflammatory disease, we evaluated whether stress exerts a sexually dimorphic effect on a major component of the inflammatory response, plasma extravasation. We evaluated the effect of a nonhabituating stress, repeated intermittent sound (30 min ⁄ day for 4 days), on neurogenic synovial plasma extravasation, induced by bradykinin in the rat knee joint. Sound stress profoundly inhibited bradykinin-induced plasma extravasation in male rats, but profoundly enhanced it in female rats. These effects took 24 h to fully develop after the last exposure to stress. In gonadectomized males, bradykinin-induced plasma extravasation was lower than intact males, and sound stress now enhanced it, i.e. gonadectomized males were phenotypically like intact females. In gonadectomized females, bradykinin-induced plasma extravasation was greater than in intact adult females, and sound stress still enhanced it. Adrenal enucleation significantly attenuated the effect of sound stress on bradykinin-induced plasma extravasation in both male and female rats. We tested the hypothesis that these effects of sound stress were due to sustained enhanced plasma levels of stress hormones. Corticosterone and epinephrine, only when administered in combination, over five days, produced a qualitatively similar effect as sound stress, i.e. bradykinin-induced plasma extravasation was significantly decreased in males and increased in females. These findings suggest that a combined effect of the hypothalamic-pituitary adrenal and sympathoadrenal stress axes are responsible for the marked sexual dimorphism in the effect of stress on the inflammatory response.

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The contribution of epinephrine to experimentally induced urethral inflammation in the rat

Cited by 12 publications

References 9 publications

Corticotropin-releasing hormone deficiency unmasks the proinflammatory effect of epinephrine

Corticotropin-releasing hormone deficiency unmasks the proinflammatory effect of epinephrine

Effects of paracetamol and etodolac on plasma adrenaline levels of rats

Sexual dimorphism in the effect of nonhabituating stress on neurogenic plasma extravasation

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