Adrenal cortical and medullary hormones in recovery of tissues from local injury

Sendelbeck, LR; Fe, Yates

doi:10.1152/ajplegacy.1970.219.4.845

Cited by 7 publications

(3 citation statements)

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“…The combination of adrenaline with dexamethasone or corticosterone in the adrenalectomized animal restores a-macrofoetoprotein production completely in a synergistic way, and less so as an additive effect. This is in accordance with other studies on experimental inflammation (Sendelbeck & Yates, 1970;Egger et al, 1982). The same was found for fibrinogen (Crane & Miller, 1977).…”

Section: Discussionsupporting

confidence: 93%

Glucocorticoids and catecholamines as mediators of acute-phase proteins, especially rat α-macrofoetoprotein

Gool¹,

Boers²,

Sala³

et al. 1984

Biochemical Journal

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Adrenal hormones were studied as possible triggering substances of the synthesis of acute-phase reactants in rats. alpha-Macrofoetoprotein, which rises sharply in concentration during inflammation, was used to monitor the acute-phase reaction. In normal rats glucocorticoids and catecholamines induce alpha-macrofoetoprotein synthesis; glucocorticoids only increase alpha-macrofoetoprotein to moderate levels in plasma, but catecholamines enhance alpha-macrofoetoprotein synthesis to very high levels, comparable with those observed in the post-injury phase. However, catecholamines in vivo also activate the adrenal cortex, suggesting a synergistic effect of both kinds of adrenal hormones. Our study showed that in adrenalectomized rats, the effect of catecholamines on alpha-macrofoetoprotein synthesis is greatly diminished, whereas the moderate effect of glucocorticoids remains. Combination of glucocorticoids and catecholamines induces extremely high alpha-macrofoetoprotein levels in both adrenalectomized and normal rats. With crossed immunoelectrophoresis it was shown that other acute-phase reactants, such as haptoglobin and alpha 1-major acute-phase protein, are affected differently by the hormones. Contrary to glucocorticoids, catecholamines give a pattern comparable with that found after surgical injury.

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Section: Discussionsupporting

confidence: 93%

Glucocorticoids and catecholamines as mediators of acute-phase proteins, especially rat α-macrofoetoprotein

Gool¹,

Boers²,

Sala³

et al. 1984

Biochemical Journal

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“…The exacerbation of inflammatory responses in adrenalectomized animals has been ascribed to a loss of endogenous glucocorticoids [11,12,34], We pro posed that following the administration of the inflam matory stimulus, C. pan'um, an increase in endoge nous glucocorticoid levels could contribute to the reduction in prostacyclin generation in activated mac rophages [9], This hypothesis was tested indirectly by comparing the effects on macrophage prostacyclin generation of in vivo pretreatment with C. parvum with in vitro treatment with dexamethasone. Although déxaméthasone reduced the basal generation of pros tacyclin in non-activated macrophages, the amount of prostacyclin produced remained higher than that gen erated by activated macrophages.…”

Section: Discussionmentioning

confidence: 99%

Regulation of Eicosanoid Generation in Activated Macrophages

Lim

Stewart²

1991

Int Arch Allergy Immunol

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Macrophage activation is accompanied by reductions in prostacyclin generation and platelet-activating factor (PAF) levels, but the mechanism has not been identified. We have investigated the involvement of glucocorticoid-sensitive mechanisms and endogenous PAF in this phenomenon. The synthetic glucocorticoid, dexamethasone (1 μM) reduced basal prostacyclin and PAF generation in resident, but not in activated macrophages. PAF receptor antagonists or dexamethasone reduced the basal, but not stimulation-induced prostacyclin generation in resident macrophages. Dexamethasone and PAF antagonists did not have synergistic inhibitory effects on prostacyclin generation by resident macrophages, and the reduction was less than that which accompanies macrophage activation. Thus, differences in the effects of PAF receptor antagonists and dexamethasone compared with macrophage activation on zymosan-induced prostacyclin synthesis indicate that factors other than PAF or glucocorticoid-sensitive mechanisms contribute to this phenomenon. Subsequent experiments with culture media conditioned by resident macrophages indicated the presence of a soluble factor which increases prostacyclin generation and appears to be absent in media conditioned by activated macrophages.

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“…This mechanism can be activated by the pituitary-adrenal axis in response to environmental situations (perhaps explaining certain aspects of the enigmatic 'counter irritant effect'), as well as by the administration of exogenous steroids. One consequence of this would be that adrenalectomized animals would be less able to terminate inflammatory reactions: there is already some evidence that this may be so (Sendelbeck & Yates, 1970).…”

Section: Discussionmentioning

confidence: 99%

Glucocorticoids Induce the Formation and Release of Anti‐inflammatory and Anti‐phospholipase Proteins Into the Peritoneal Cavity of the Rat

Blackwell¹,

Carnuccio

Rosa

et al. 1982

British J Pharmacology

205

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1 Dexamethasone and hydrocortisone induce the release of anti-phospholipase proteins into the peritoneal cavities of rats. 2 Adrenocorticotrophic hormone (ACTH) also releases these proteins in normal but not in adrenalectomized rats. 3 Peritoneal lavage proteins were separated by ion-exchange and size exclusion chromatography. The anti-phospholipase activity occurred in four separate fractions with the major component having an apparent mol.wt. of 40 k. 4 Column fractions containing these anti-phospholipase proteins had anti-inflammatory effects in the rat carrageenin pleurisy model whereas other fractions were inactive. 5 The proteins appear to be identical to macrocortin and lipomodulin, the 'second messengers' of glucocorticoid hormone action on the arachidonate system.

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Adrenal cortical and medullary hormones in recovery of tissues from local injury

Cited by 7 publications

References 0 publications

Glucocorticoids and catecholamines as mediators of acute-phase proteins, especially rat α-macrofoetoprotein

Glucocorticoids and catecholamines as mediators of acute-phase proteins, especially rat α-macrofoetoprotein

Regulation of Eicosanoid Generation in Activated Macrophages

Glucocorticoids Induce the Formation and Release of Anti‐inflammatory and Anti‐phospholipase Proteins Into the Peritoneal Cavity of the Rat

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