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Regulation of the HPA axis by alpha 2 adrenoceptors
Author(s) -
HemrickLuecke Susan Kay,
Thompson Linda K,
Zink Charity,
Marlow Deanna L,
Rathmell Richard E
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a790-a
Subject(s) - idazoxan , autoreceptor , guanfacine , clonidine , endocrinology , antagonist , medicine , chemistry , corticosterone , alpha (finance) , norepinephrine , adrenergic receptor , guanabenz , pharmacology , agonist , dopamine , receptor , prazosin , hormone , construct validity , nursing , patient satisfaction
The hypothalamic‐pituitary‐adrenal (HPA) axis is regulated by numerous neurotransmitters, including central norepinephrine (NE), which exerts a stimulatory role on the HPA axis. There are numerous adrenoceptors (AR) subtypes involved in the regulation of the effects on NE, including 3 subtypes of alpha (α)2 ARS –α2A, α2B and α2C. While no evidence exists for a specific role of α2B ARs in regulation of central NE release, α2A and α2C ARs exist as presynaptic autoreceptors mediating NE neurotransmission. We investigated the role of the non‐selective α2 antagonists RX821002 and idazoxan, a selective α2A antagonist BRL 44408 and a selective α2C antagonist OPC 28326 in blocking increases in rat plasma corticosterone levels produced by the α2 AR agonists clonidine and guanfacine. Corticosterone levels were increased 1 hour after systemic administration of both clonidine and guanfacine, which were dose‐dependently blocked by both selective and non‐selective α2 AR antagonists. These data suggest that both α2A and α2C ARs regulate the effects of NE on the HPA axis. Further studies on the in vivo effects of α2A and α2C ARs are needed to elucidate the functional activity of α2 ARs.