Neural control of adrenocortical secretion

A variety of neural sensory stimuli as well as the stimulation of extrahypothalamic structures can produce an increase in ACTH and corticosterone (CS) secretion. This effect is mediated, at least partially, by corticotropin releasing factor (CRF)-41. Experiments involving stimulation, brain lesions and hypothalamic deafferentations have demonstrated that the mechanisms responsible for this activation are not uniform and the effects of the various modalities are mediated by different pathways. In addition to the anterior hypothalamic input, which plays an important role in the mediation of the adrenocortical responses, the medial forebrain bundle as well as a medial posterior hypothalamic input are also essential for the activation of the hypothalamo-pituitary-adrenocortical axis for some neural modalities. Norepinephrine (NE) seems to have a facilitatory effect on these mechanisms as depletion of hypothalamic NE blocks the rise in serum CS following both peripheral and central neural stimuli. This effect is mediated by alpha 1 and alpha 2 adrenoceptors, the role of beta receptors being unclear. NE palsy also an important role in the early and late changes of CRF-41 content in the median eminence and serum ACTH following adrenalectomy.