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1 a result of adrenal hypersensitivity toward adrenocorticotropin.
2 xpression in hypothalamic neurons regulating adrenocorticotropin.
3 es to release prolactin, growth hormone, and adrenocorticotropin.
4 of H4, but not an H3 peptide nor the peptide adrenocorticotropin.
5 -butyryl cyclic adenosine monophosphate, and adrenocorticotropin.
6 the pituitary and it was poorly processed to adrenocorticotropin.
7 in, and peptide fragments of substance P and adrenocorticotropin.
9 and female rats, with females secreting more adrenocorticotropin (ACTH) and corticosterone than males
10 mulate the secretions of prolactin (PRL) and adrenocorticotropin (ACTH) and to inhibit the secretion
11 equations which include pulsatile release of adrenocorticotropin (ACTH) by the pituitary gland and a
13 homeostasis are accompanied by increases in adrenocorticotropin (ACTH) concentrations in fetal perip
14 he human adrenal cortex, the peptide hormone adrenocorticotropin (ACTH) directs cortisol and adrenal
15 ted after a variety of stimuli that increase adrenocorticotropin (ACTH) in the systemic circulation.
17 elanocortin (POMC), the common precursor for adrenocorticotropin (ACTH) of pars distalis corticotrope
20 selective agonists on the corticosterone and adrenocorticotropin (ACTH) response to immobilization st
23 hypothalamus attenuate, but do not abolish, adrenocorticotropin (ACTH) secretion in response to acut
25 of S203 phosphorylation and is unaffected by adrenocorticotropin (ACTH) treatment, loss of SUMOylatio
26 Brachiocephalic occlusion (BCO) stimulated adrenocorticotropin (ACTH), cortisol and arginine vasopr
27 hesis in the adrenal cortex is controlled by adrenocorticotropin (ACTH), which increases intracellula
29 90% of all budesonide patients had a normal adrenocorticotropin (ACTH)-stimulated cortisol response
31 ondrial movement, by which activation of the adrenocorticotropin (ACTH)/cAMP signaling pathway stimul
32 2)-melanocyte stimulating hormones (MSH) and adrenocorticotropin (ACTH)], the antagonist agouti-relat
33 ncy (FGD), or hereditary unresponsiveness to adrenocorticotropin (ACTH; OMIM 202200), is an autosomal
35 n (POMC)-derived peptides (the melanocortins adrenocorticotropin, alpha-, beta- and gamma-melanocyte
37 muscarinic antagonist Scopolamine augmented adrenocorticotropin and corticosterone responses to rest
39 and 2DG exhibited increased levels of plasma adrenocorticotropin and corticosterone, indicating that
41 HPA axis assessment included monitoring of adrenocorticotropin and cortisol over a full circadian c
42 l activity was monitored by measuring plasma adrenocorticotropin and cortisol, 24 hr urinary cortisol
43 iencies include growth hormone, thyrotropin, adrenocorticotropin and gonadotropin deficiencies, prima
44 outing and secretion of pro-opiomelanocortin/adrenocorticotropin and growth hormone from anterior pit
45 , the anterior lobe corticotropes, producing adrenocorticotropin, and the intermediate lobe melanotro
46 nt increase in circulating concentrations of adrenocorticotropin, cortisol, and norepinephrine after
47 of the corticotropin-releasing hormone (CRH)-adrenocorticotropin-glucocorticoid axis, mediated by the
48 paraventricular nucleus (PVN), the pituitary adrenocorticotropin hormone (ACTH) and adrenal corticost
51 adrenocortical (HPA) axis and the release of adrenocorticotropin hormone (ACTH) and corticosterone in
52 holino-sydnonimine (SIN-1) on the release of adrenocorticotropin hormone (ACTH) and the neuronal resp
53 plasma concentrations of corticosterone and adrenocorticotropin hormone (ACTH) are unchanged, and a
54 ng inflammation CRH is required for a normal adrenocorticotropin hormone (ACTH) increase but not for
59 re analyzed for pro-opiomelanocortin (POMC), adrenocorticotropin hormone (ACTH), alpha-MSH, beta-MSH,
66 treated with conventional therapies such as adrenocorticotropin hormone, corticosteroids, and/or int
70 of alpha-melanocyte stimulating hormone and adrenocorticotropin in the epidermis and melanocytes has
71 a cascade of events which culminates in the adrenocorticotropin-induced release of corticosteroids f
72 only a modest elevation of their concurrent adrenocorticotropin levels (57 +/- 13 vs. 29 +/- 9 pmol/
73 t stress, whereas their plasma and pituitary adrenocorticotropin levels were either unchanged or lowe
74 one to cortisol does not occur, resulting in adrenocorticotropin-mediated androgen excess and a pheno
75 ycytes rarely contained detectable levels of adrenocorticotropin or alpha-melanocyte-stimulating horm
76 gainst alpha-melanocyte stimulating hormone, adrenocorticotropin, prohormone convertases 1 and 2 (PC1
78 ccompanied by elimination of the exaggerated adrenocorticotropin responses to a saline injection (min
80 PDE8s have their greatest control under low adrenocorticotropin-stimulated conditions, whereas other
81 elective inhibitor (PF-04957325) potentiates adrenocorticotropin stimulation of steroidogenesis by in
83 eveloped a protocolized approach to low-dose adrenocorticotropin testing and empirical low-dose gluco
84 sor-dependent shock receiving protocol-based adrenocorticotropin testing and low-dose steroid supplem
89 enzyme 2, which catalyzes the conversion of adrenocorticotropin to alpha-MSH, thereby decreasing alp
90 , and CSF cortisol were elevated, and plasma adrenocorticotropin was reduced in the active treatment