Glucocorticoid action: a mechanism involving nuclear and non-nuclear pathways

Johnson, Lorin K.; Longenecker, John P.; Baxter, John D.; Dallman, Mary F.; Widmaier, Eric P.; Eberhardt, Norman L.

doi:10.1111/j.1365-2133.1982.tb01026.x

Cited by 52 publications

(22 citation statements)

References 60 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is possible glucocorticoids play a role by: (i) limiting the inflammation caused by debris generated during the procedure or (ii) minimizing healing of the ventriculostomy, both known mechanisms of action for this family of drugs (11,18). The majority of these patients, who presented with uncompensated obstructive hydrocephalus, were given perioperative steroids to treat peritumoral edema in the setting of a new tumor diagnosis.…”

Section: Peer-review Reportsmentioning

confidence: 98%

Predictors of Surgery-Free Outcome in Adult Endoscopic Third Ventriculostomy

Woodworth¹,

See²,

Bettegowda³

et al. 2012

World Neurosurgery

View full text Add to dashboard Cite

Section: Peer-review Reportsmentioning

confidence: 98%

Predictors of Surgery-Free Outcome in Adult Endoscopic Third Ventriculostomy

Woodworth¹,

See²,

Bettegowda³

et al. 2012

World Neurosurgery

View full text Add to dashboard Cite

“…Corticosteroids speci cally bind to cytosolic glucocorticoid receptors, nally resulting in an increase or decrease of gene transcription. In addition, non-genomic receptor-mediated or non-speci c effects, as well as membrane receptor-mediated processes, are involved in corticosteroid action (6,7).…”

mentioning

confidence: 99%

Corticosteroids Impair Intestinal Epithelial Wound Repair Mechanisms In Vitro

Jung¹,

Fehr²,

Harder-D'heureuse³

et al. 2001

Scandinavian Journal of Gastroenterology

View full text Add to dashboard Cite

show abstract

“…8 Similar inhibition of gene transcription has been reported for the interleukin β gene. 9 In addition, glucocorticoids produce relatively rapid reduction of corticotropin (adrenocorticotropic hormone, ACTH) release before demonstrable effects of corticotropin biosynthesis, 10,11 as well as rapid inhibition of basal or circadian release of corticotropin-releasing hormone (CRH) from hypothalamus and CRH-stimulated release of corticotropin from the pituitary. 8,12,13 This rapid inhibition is not affected by pretreatment with cycloheximide in a dose that inhibits protein synthesis.…”

mentioning

confidence: 99%

Pharmacokinetics and pharmacodynamic modeling of direct suppression effects of methylprednisolone on serum cortisol and blood histamine in human subjects

Kong

Ludwig

Slaughter

et al. 1989

Clin Pharmacol Ther

View full text Add to dashboard Cite

Pharmacodynamic models for "directly suppressive" effects of methylprednisolone are based on the premise that receptor interactions of steroids are followed by immediate suppression of either the circadian secretion of cortisol or the constant rate recirculation of histamine-containing basophils that persists until inhibitory concentrations of methylprednisolone disappear. Methylprednisolone doses of 0, 10, 20, and 40 mg were given as the 21-succinate sodium salt in a balanced crossover study to six normal men. Plasma steroid concentrations and blood histamine were measured simultaneously. Both forms of methylnisolone exhibited linear kinetic parameters. One dynamic model quantitates the baseline circadian pattern and the decline and return of cortisol with similar parameter estimates for all three dose levels. A similar model describes the monoexponential decline and the log-linear return to steady-state baseline of blood histamine. Similar inhibitory concentration values for both effects approximated the equilibrium dissociation constant of in vitro steroid receptor binding. The new models are more physiologically appropriate for these steroid effects than three other models that are commonly employed in pharmacodynamics. Steroid effects generally appear to be receptor mediated with either nongene immediate responses or gene-mediated delayed effects. These models allow quantitation of the rapid effects of steroids with simple equations and common fitted parameters for all steroid dose levels.The diverse immunosuppressive and the antiinflammatory effects of glucocorticoids in human beings complicate the development of realistic and comprehensive kinetic and dynamic models for this class of agents. This is partly because of the complex mode of action of corticosteroids, which involves receptor binding and the formation of second messengers and proteins (which is mediated by deoxyribonucleic acid [DNA]). Such responses are typically characterized by a slow and delayed induction period. This receptorReprint requests: William J. Jusko, PhD, 565 Hochstetter Hall, School of Pharmacy, State University of New York at Buffalo, Buffalo, NY 14260. Presented in part at the Third Annual Meeting of American Association of Pharmaceutical Scientists (AAPS), Orlando, Florida, Oct. 30 to Nov. 3, 1988. NIH Public Access Author ManuscriptClin Pharmacol Ther. Author manuscript; available in PMC 2014 October 23. Published in final edited form as:Clin Pharmacol Ther. 1989 December ; 46(6): 616-628. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript gene mode of action has been successfully modeled for prednisolone effects in rats. 1,2 In human beings, pharmacodynamic modeling of glucocorticoid responses has focused on Sheiner's model 3 of linkage of a hypothetical "effect compartment" to the plasma concentration. This approach has been used to characterize the fall and return of OKT3-and OKT4-positive lymphocytes in peripheral blood after single oral doses of prednisolone. 4 A threshold concentratio...

show abstract

Glucocorticoid action: a mechanism involving nuclear and non-nuclear pathways

Cited by 52 publications

References 60 publications

Predictors of Surgery-Free Outcome in Adult Endoscopic Third Ventriculostomy

Predictors of Surgery-Free Outcome in Adult Endoscopic Third Ventriculostomy

Corticosteroids Impair Intestinal Epithelial Wound Repair Mechanisms In Vitro

Pharmacokinetics and pharmacodynamic modeling of direct suppression effects of methylprednisolone on serum cortisol and blood histamine in human subjects

Contact Info

Product

Resources

About