I wonder if aside from a peripheral effect mediated via glucocorticoid receptors, there is a feedback mechanism, ACTH production will be suppressed by glucocorticoids, and ACTH comes from a common precursor peptide, proopiomelanocortin, which gets sliced and diced into various peptides, including ACTH, beta-endorphin, and the melanocyte stimulating hormones.
With how finely tuned the body's homeostatic mechanisms are, I would be most surprised if a simple reduction in POMC transcription would be the sole way that ACTH secretion is regulated, aside from causing decrease in CRF release (and probably interactions with CRF-binding protein, which acts as a sink for excess CRF, although its function is considerably more in depth than that, apparently)...I am just studying that area of biochemistry actually, because my g/f has a severe corticosteroid deficiency, due to lack of ACTH, most likely stemming from a hypothalamic issue causing greatly decreased capacity for CRF production or release.
I wonder, if aside from glucocorticoid mediated suppression of CRF release, there are interactions with the enzymes that are required to split POMC into ACTH, beta-endorphin and the melanocyte stimulating hormones.
I might try a dose or two of hydrocortisone and try and appraise its effects on opioid withdrawal, because worse luck, I am there right now, and its pissing me off, tapering down on dihydrocodeine, which I use for a knee condition, temporarily to get my tolerance down and eliminate physical dependence. So far I have cut my dose by 3/4, then switched to a Mu1 selective partial agonist, if I can find it...I know I have some around here somewhere.
http://www.ncbi.nlm.nih.gov/pubmed/7652513
Different Opioid Mechanisms Are Involved in the Modulation of ACTH and Gonadotrophin Release in Man.
Neuroendocrinology 1986;42:357-360 (DOI: 10.1159/000124463)