ABSTRACT
It is well established that the mechanisms which modulate adrenocorticotropic hormone (ACTH) secretion by the pituitary involve the interaction of several secretagogues. In addition, arginine-vasopressin, catecholamines, and angiotensin-II also act on the pituitary to increase the release of ACTH, but their effect is highly dependent upon the presence of endogenous corticotropin releasing factor (CRF) with which they exert an additive or synergetic action. The high potency and intrinsic activity exhibited by CRF to stimulate the release of ACTH has been established in a number of in vitro and in vivo models. The in vivo ability of CRF administered by intravenous, subcutaneous or cerebroventricular routes to increase ACTH secretion has been established in several species, including rat, sheep, primates, and man. The negative feedback exerted by glucocorticoids on ACTH secretion is well established and has been extensively discussed. In cultured pituitary cells, as well as in the intact rat, corticosteroids interfere with the stimulatory action of CRF in a dose-dependent manner.
