The effect of different α2-adrenoreceptor subtype agonists and antagonists on adrenocorticotrop hormone (ACTH) and β-endorphin release induced by ether stress was examined. Ether inhalation-induced ACTH and β- endorphin increase was inhibited by ICV administration of 30 μg but not 1 and 10 μg clonidine (α2-adrenoreceptor agonist). ICV oxymetazoline (α(2A)-adrenoreceptor agonist; 1-10-30 μg) or the α1-agonist methoxamine (100 μg/rat) failed to inhibit the stress-induced rise. Pretreatment with the α1/α2(2B,C)-antagonist prazosin (0.5 mg/kg, IP) prevented the effect of clonidine on the ether stress, while the α1/α(2A)-antagonist WB-4101 (0.5 mg/kg, IP) was unable to counteract the inhibitory effect of clonidine. Prazosin alone had no effect on the ether-induced plasma ACTH and β- endorphin elevation. These results suggest that noradrenaline in the central nervous system may inhibit the stress-induced hypothalamo-pituitary-axis and pituitary β-endorphin activation via α(2B,C)-adrenoceptor subtypes and prazosin may antagonize its effect on these receptors.
- Ether stress
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Endocrine and Autonomic Systems
- Psychiatry and Mental health
- Biological Psychiatry