Abstract
The endocrine stress response is influenced by the corticotrophin‐releasing hormone (CRH) family of peptides, with Urocortin 2 (Ucn2) implicated in the regulation of adrenomedullary catecholamine synthesis and release. Here, we examined the effect of immobilization stress (IMO) on gene expression of CRH family members in rat adrenal medulla. Basal Ucn2 mRNA levels were several orders of magnitude higher than CRH, Ucn1 and CRH receptors, and Ucn3 mRNA was undetectable. IMO increased Ucn2 gene expression >;30 fold and also raised CRH mRNA levels, albeit to a lesser extent (6 fold). Involvement of glucocorticoids was studied. Treatment of PC12 cells with dexamethasone greatly increased Ucn2 mRNA levels in a dose‐dependent manner, a response abolished by pretreatment with transcription inhibitor, actinomycin D. Modest changes in CRH receptor type 1 (CRHR1) and type 2 (CRHR2) were also observed. Moreover, IMO did not induce Ucn2 mRNA in CRH knockout mice. The results suggest that the stress‐triggered rise in glucocorticoids stimulates a large induction of Ucn2 mRNA levels which may allow Ucn2 to act in an autocrine/paracrine fashion to modulate adrenomedullary function, or act as an endocrine hormone. Supported by American Heart Association grant 10GRNT4420001 and Slovak grants APVV‐0088–10 and VEGA 2/0036/11.
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