Treatment of fetal rats and embryonic chickens with exogenous glucocorticoids induces premature growth hormone (GH) cell differentiation. However, it is unknown whether the developing adrenal gland is capable of mounting this response autonomously. The present study determined whether stimulation of the adrenal gland in developing chicken embryos through administration of adrenocorticotropic hormone (ACTH) could induce a premature increase in GH cells. We found that plasma corticosterone and ACTH levels increased between embryonic day (e) 11 and e17, consistent with GH cell (somatotroph) ontogeny. Injection of ACTH into eggs on e9, e10, or e11 increased somatotrophs on e14. In contrast, thyroid-stimulating hormone, corticotropin-releasing hormone, -melanocyte-stimulating hormone, GH-releasing hormone, and thyrotropin-releasing hormone were ineffective. Culture of e11 pituitary cells with ACTH failed to induce somatotrophs, suggesting an indirect action of ACTH on GH cells in vivo. Intravenous administration of ACTH dramatically increased plasma levels of corticosterone within 1 hour and increased the percentage of pituitary somatotrophs within 24 hours. Although ACTH administration increased the relative abundance of pituitary GH cells, there was no effect on plasma levels of GH, insulin-like growth factor (IGF)-I, or IGF-II or in hepatic expression of IGF-I or IGF-II mRNA. We conclude that ACTH administration can increase the population of GH cells in the embryonic pituitary. However, this treatment alone does not lead to downstream activation of hepatic IGF production. These findings indicate that the embryonic adrenal gland, and ultimately anterior pituitary corticotrophs, may function to regulate pituitary GH cell differentiation during embryonic development.