Glucocorticoids act within the pituitary gland to maintain the blood levels of glucocorticoids within appropriate limits by negative feedback on the secretion of corticotrophin (ACTH). Annexin 1 (ANXA1) is a calcium- and phospholipid binding protein which was originally identified as a mediator of the anti-inflammatory actions of glucocorticoids in the host defence system. Subsequent work has shown that it that plays an important role in the early delayed (30 min-3 h) feedback effects of glucocorticoids in the pituitary on ACTH and prolactin, GH and TSH secretion. ANXA1 is not expressed by classical secretory cells in the pituitary but is abundant in folliculostellate cells. Glucocorticoids and other stimuli (e.g. ATP) act on folliculostellate cells to cause translocation of ANXA1 to the plasma membrane, with particular accumulation at points where the cells make contact with secretory cells. This process is effected via a non-genomic mechanism and is dependent upon PKC-dependent serine-phosphorylation of ANXA1, lipidation, blockade of ATP-sensitive-K+ channels and an ATP-binding cassette transport protein, ABCA1. The released protein then acts via cell surface receptors on the adjacent secretory cells to suppress stimulus-evoked peptide release. Our recent data suggest that the receptor on the secretory cells is a member of the G-protein coupled formyl peptide receptor (FPR) family.