EVIDENCE FOR 6-KETO-PGF1-ALPHA IN ADRENAL-CORTEX OF THE RAT AND EFFECTS OF 6-KETO-PGF1-ALPHA AND PGI2 ON ADRENAL CAMP LEVELS AND STEROIDOGENESIS

Both intact cortical tissue and isolated cortical cells from the adrenal gland of the rat were analyzed for 6-keto-PGF1α, the hydrolysis metabolite of PGI2, using high-performance liquid chromatography and gas chromatography-mass spectrometry. 6-Keto-PGF1α was present in both incubations of intact tissue and isolated cells of the adrenal cortex, at higher concentrations than either PGF2α or PGE2. Thus, the cortex does not depend upon vascular components for the synthesis of the PGI2 metabolite. Studies in vitro, using isolated cortical cells exposed to 6-keto-PGF1α (10-6-10-4M), show that this PG does not alter cAMP levels or steroidogenesis. Cells exposed to PGI2 (10-6-10-4M), however, show a concentration-dependent increase of up to 4-fold in the levels of cAMP without altering corticosterone production. ACTH (5-200 μU/ml) increased cAMP levels up to 14-fold, and corticosterone levels up to 6-fold, in isolated cells. ACTH plus PGI2 produced an additive increase in levels of cAMP, however, the steroidogenic response was equal to that elicited by ACTH alone. Adrenal glands of the rat perfused in situ with PGI2 showed a small decrease in corticosterone production, whereas ACTH greatly stimulated steroid release. Thus, while 6-keto-PGF1α is present in the rat adrenal cortex, its precursor, PGI2, is not a steroidogenic agent in this tissue although it does stimulate the accumulation of cAMP. © 1979.