Central catecholaminergic control of ACTH secretion

https://doi.org/10.1016/0167-0115(88)90013-4Get rights and content

Abstract

Plasma adrenocorticotropic hormone (ACTH) has been measured after an intra-third ventricular administration of noradrenaline, an adrenergic agonist or an adrenergic antagonist. Centrally administered noradrenaline caused a significant increase in ACTH secretion. The α-agonist phenylephrine also increased the ACTH level. However, neither the α-antagonist phentolamine nor β-agonist isoproterenol affected the ACTH level. The β-antagonist propranolol evoked a significant elevation in ACTH. Passive immunoneutralization was examined with anti-rat corticotropin-releasing factor (CRF) rabbit serum, anti-arginine vasopressin (AVP) rabbit serum and normal rabbit serum (NRS) on the intra-third ventricular noradrenaline-induced ACTH secretion to study the involvement of endogenous CRF. An intra-third ventricular administration of noradrenaline caused a significant increase of ACTH levels in NRS-injected rats and anti-AVP-injected rats, whereas an i.v. anti-rat CRF injection significantly reduced the intra-third ventricular noradrenaline-induced ACTH secretion. These results suggest that central catecholamine stimulated ACTH secretion via the α-adrenergic mechanism and that endogenous CRF is at least partly involved in the noradrenaline-induced ACTH secretion.

References (28)

  • T.A. Day et al.

    Noradrenergic afferents facilitate the activity of tuberoinfundibular neurons of the hypothalamic paraventricular nucleus

    Neuroendocrinology

    (1985)
  • S. Al-Damluji et al.

    Alpha-adrenergic stimulation of corticotropin secretion by a specific central mechanism in man

    Neuroendocrinology

    (1987)
  • C. Rivier et al.

    Modulation of stress-induced ACTH release by corticotropin-releasing factor, catecholamines and vasopressin

    Nature (Lond.)

    (1983)
  • D.A. Bereiter et al.

    Caudolateral areas of medulla-mediating release of ACTH in cats

    Am. J. Physiol.

    (1986)
  • Cited by (30)

    • Hypothermic responses to infection are inhibited by α<inf>2</inf>- adrenoceptor agonists with possible clinical implications

      2009, British Journal of Anaesthesia
      Citation Excerpt :

      Infusion of either the α2-agonists or the antagonists failed to affect basal or LPS-stimulated plasma corticosterone levels. This result was unexpected, since several previous studies have demonstrated a role for α2-adrenoceptors in the regulation of the HPA axis.37–42 Hence α2-agonists and antagonists have been shown to, respectively, attenuate and augment basal and stimulated adrenocorticotrophic hormone (ACTH) and corticosterone responses.37 38 43

    • Progressive dysregulation of autonomic and HPA axis functions in HIV-1 clade C infection in South India

      2008, Psychoneuroendocrinology
      Citation Excerpt :

      This sequential neuroendocrine regulatory pathway thus prevents the deleterious effects of stress on the brain (Sapolsky et al., 1986; Sapolsky, 1996). Although the exact mechanisms involving the disconnect between the attenuated response of ACTH, and hyper response of cortisol to star tracing challenge in HIV-1C infected individuals is not clearly understood at present, it may be suggested that it is a reflection of an attenuated noradrenergic response to MSTCT found in this study, since the release of ACTH from the pituitary is also stimulated by the noradrenergic system (Takao et al., 1988). Similar findings from other studies also suggest that autonomic response to life events regulate the HPA axis activity and that integration of the central autonomic system with CNS is essential for the activation of the HPA axis (Malarkey et al., 1994).

    View all citing articles on Scopus
    View full text