Estradurin (a polymer of 17-beta-oestradiol) has an inhibitory effect on the synthesis/secretion of PRL. This effect is assumed to be caused by the strong inhibitory effect of the drug on phosphatases. With increasing time of low doses of Estradurin (0.001 micrograms/ml) in vitro, the inhibitory effect on PRL secretion was overcome and the synthesis/secretion of PRL increased. The secretion of GH was unaffected in all concentrations (0.001-0.1 micrograms/ml) except 1 microgram/ml. A stimulatory effect of 17-beta-oestradiol (0.01 micrograms/ml) on the synthesis/secretion of PRL was suggested by the tissue from one post-pregnancy pituitary. Short time organ cultures from prolactinomas or tumors with a concomitant secretion of GH and PRL show no changes of GH or PRL secretion following incubation with (0.001-0.1 micrograms/ml) of 17-beta-oestradiol. However, electron microscopy of 17-beta-oestradiol incubated specimens revealed an increased number of lysosomes and inclusion bodies in the cell cytoplasm. Incubation with testosterone (0.001-1 microgram/ml) cause inhibition of PRL synthesis/secretion in two of three prolactinomas. In GH secreting tumours testosterone did not effect PRL or GH secretion in vitro when compared with controls. The ultrastructural analysis of specimens in which a decrease of PRL synthesis/secretion had occurred showed myelin figures in the cell cytoplasm and accumulations of amorphous electron dense inclusion bodies.