INDUCTION OF 20ALPHA-HYDROXYSTEROID DEHYDROGENASE IN RAT CORPORA LUTEA BY PHARMACOLOGICAL BLOCKADE OF PITUITARY PROLACTIN SECRETION

1. 1. The enzyme 20α-hydroxysteroid dehydrogenase was assayed in vitro in ovaries from rats treated during pseudopregnancy or early pregnancy with various ergot alkaloids used independently or in conjunction with ovine pituitary prolactin. Localization of 20α-hydroxysteroid dehydrogenase was examined histochemically. 2. 2. Ergocornine, a drug believed to block the release of prolactin from the pituitary, induced a 3-4 fold rise in enzyme activity in the ovary as a whole; in the corpora lutea of pregnancy the induced rise was about 100-fold. This action was prevented by exogenous prolactin. 3. 3. Neither ergocornine nor prolactin affected 20α-hydroxysteroid-dehydrogenase activity when added in vitro to the assay system, excluding a direct interaction with the enzyme protein as the basis of their action in vivo. 4. 4. The ability of ergot drugs to induce a rise in ovarian 20α-hydroxysteroid dehydrogenase was closely correlated with their ability to interrupt the progestational state. 5. 5. Newly-formed cyclic corpora lutea and corpora lutea graviditatis were devoid of histochemically demonstrable 20α-hydroxysteroid dehydrogenase, but activity appeared in the cyclic corpora toward the end of dioestrus. Involuting corpora, and corpora of rats treated with ergocornine during early pregnancy, were strongly positive for 20α-hydroxysteroid dehydrogenase. 6. 6. It was concluded that prolactin suppresses the synthesis of 20α-hydroxysteroid dehydrogenase in corpora lutea and that this hormone may owe part of its luteotrophic" action in the rat to this effect. We suggest that physiological or druginduced prolactin deprivation over a critical period irreversibly induces 20α-hydroxysteroid-dehydrogenase synthesis in the luteal cell and thus reduces its ability to secrete progesterone. © 1969."