Disease relevance of CRH

• After CRH administration, the increment in plasma ACTH was significantly (p < 0.05) lower in dogs with pituitary-dependent hyperadrenocorticism (221 +/- 53 ng/l) than that in control dogs (279 +/- 41 ng/l) [1].
• In conclusion, canine corticotrophic adenomas are less sensitive to stimulation by CRH and less sensitive to inhibition by glucocorticoids [2].
• Therefore, stimulation with CRH produced 2 patterns of plasma IR-ACTH response when administered to dogs with naturally acquired adrenal insufficiency [3].
• Of the 7 dogs with primary adrenal insufficiency, 6 had markedly high basal plasma IR-ACTH concentrations and exaggerated ACTH responses to CRH administration, whereas 1 dog that was receiving replacement doses of prednisone at the time of testing had normal basal IR-ACTH concentrations and a nearly normal response to CRH [3].
• Responsiveness to corticotropin-releasing hormone and vasopressin in canine Cushing's syndrome [1].

High impact information on CRH

• In the old dogs, the stress- and CRH-induced cortisol peaks were relatively higher than those of ACTH, and their adrenals weighed significantly more, suggesting chronic hyperadrenocorticotropism [4].
• After stress by immobilization as well as by light electric foot shocks and after i.v. administration of 1 microgram/kg CRH, the old dogs had higher peak levels of ACTH and cortisol, but not of alpha MSH [4].
• The CRH-induced ACTH secretion by corticotrophic adenoma cells was significantly (P < 0.05) lower than that by normal pituitary cells after 4 h incubation with CRH [2].
• CRH, AVP, IGF-I and cortisol had no effect on the proliferation of canine pituitary cells or canine corticotrophic adenoma cells [2].
• For the purpose of obtaining an integral picture of anterior pituitary function in canine pituitary-dependent hyperadrenocorticism (PDH), 47 dogs with PDH and eight control dogs received combined administration of four hypophysiotropic hormones (CRH, GHRH, GnRH and TRH) and measurements were made of ACTH, cortisol, GH, LH, PRL and TSH [5].

Chemical compound and disease context of CRH

• The ACTH secretion by corticotropic cells in pituitary-dependent hyperadrenocorticism was relatively less sensitive to stimulation with CRH than with LVP [1].

Biological context of CRH

• The AUC of the plasma cortisol vs. time curve following CRH stimulation, a measure of adrenal suppression, was reduced significantly after topical application of BMV compared with the pretreatment values [6].

Anatomical context of CRH

• Preliminary data confirmed the existence of the highest cross-reactivity of a canine hypothalamus extract, known to have a high content of CRH, with antisera directed against human, rat CRH [7].
• The CRH gene was amplified from genomic DNA obtained from white blood cells by a polymerase chain reaction and subsequently sequenced using the dideoxy method [7].
• Upon presentation of a dog, CRH increased in the amygdala of the sheep and then fell off [8].
• Repeated stress also produced an exaggeration in both of the CRH peaks to presentation of a subsequent novel stress (a forelimb electric shock) [8].
• After CRH stimulation testing and MRI, dogs were euthanatized and the pituitary gland and adrenal glands were excised for gross and histologic examination [9].

Associations of CRH with chemical compounds

• In contrast, DEX + DOM-treated dogs had daily mean ACTH concentrations ranging from 10 +/- 8.1 to 32 +/- 26 pg/ml and mean peak post-CRH ACTH concentrations of 174 +/- 16 pg/ml [10].
• Corticotropin-releasing hormone (CRH) and vasopressin are the most important hypothalamic factors regulating adrenocorticotropic hormone (ACTH) secretion [1].
• These results support a role for CRH in the physiologic regulation of ACTH secretion from the canine anterior pituitary, but do not support regulatory roles for AVP, OT, or AII [11].
• Two weeks after termination of daily prednisone administration, significant difference between group means was not evident in baseline ACTH or cortisol values, post-CRH ACTH or cortisol values, or post-ACTH cortisol values, compared with values in controls [12].
• Compared with separate administration, the combined administration of these four hypothalamic releasing hormones caused no apparent inhibition or synergism with respect to the responses to CRH, GHRH, and TRH [13].

Analytical, diagnostic and therapeutic context of CRH

• RESULTS: ACTH concentrations in mitotane treatment group dogs were significantly higher than in the control group dogs following CRH stimulation [9].
• Immunosensor-based microdialysis probes were used to measure CRH and cortisol in the amygdala and cortisol systemically in sheep exposed to a predator stress (a dog) [8].
• Oral administration of RCB did not suppress adrenocortical function, whereas BMV induced almost complete suppression of basal and CRH-induced cortisol concentrations [6].
• METHODS: Biological specificity was evaluated by treatment of 3 dogs with ovine corticotropin-releasing hormone (CRH) followed by serial measurements of ACTH and by comparison with a previously validated immunoradiometric assay [14].

References