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The biologic activity of ACTH and related peptides on peripheral blood mononuclear cells is altered by the presence of dexamethasone.

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TLDR
It was found that in the absence of dex only the peptide ACTH altered proliferation of PBMCs while there was no effect of peptide on T-cells activated via protein kinase C-mediated pathways and under certain circumstances ACTH may protect the immunologic response from the inhibitory effects of elevated ambient glucocorticoids.
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Adrenal insufficiency occurring during septic shock: incidence, outcome, and relationship to peripheral cytokine levels

TL;DR: A trend toward lower IL-6 levels in AI suggests a link between reduced IL- 6 levels and understimulation of the pituitary-adrenal axis in this group, and glucocorticoid supplementation appeared to improve short-term survival when AI occurred.
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Alcohol stimulates ACTH secretion in the rat: mechanisms of action and interactions with other stimuli.

TL;DR: The activity of the HPA axis is influenced by exposure to EtOH during embryonic development, with mature offspring showing hyporesponsiveness to many stimuli, and altered responses appear to be caused in part by changes in the synthesis/release CRF, possibly under the influence of nitric oxide.
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Restraint stress-induced thymic involution and cell apoptosis are dependent on endogenous glucocorticoids

TL;DR: Findings indicate that endogenous glucocorticoids are involved in the restraint-induced effects on the thymus.
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Direct activating effects of adrenocorticotropic hormone (ACTH) on brown adipose tissue are attenuated by corticosterone

TL;DR: Results show that ACTH activates BAT and browning of WAT while corticosterone counteracts this, and direct activating effects of adrenocorticotropic hormone (ACTH) on brown adipose tissue are attenuated by cortic testosterone.
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Sprague-Dawley rats obtained from different vendors exhibit distinct adrenocorticotropin responses to inflammatory stimuli.

TL;DR: Results show that Sprague-Dawley rats obtained from different commercial sources can differ in immune-neuroendocrine responses to inflammatory stimuli.
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