Regulation of responsiveness of cultured adrenal cells to adrenocorticotropin and prostaglandin E1: cell density, cell division, and inhibitors of protein synthesis.
In cultured bovine adrenocortical cells, responsiveness to ACTH, as assessed by the maximal rate of ACTH-stimulated cAMP production, has been found to depend on cell density and cell proliferation, while the maximal rate of prostaglandin E1 (PGE1)-stimulated cAMP production was constant. The combination of low cell density and normal cell proliferation caused a specific decline in responsiveness to ACTH. Responsiveness did not decline at any density when proliferation was inhibited by mitomycin C treatment. Specific declines in responsiveness to ACTH were also seen when cultures were treated with cycloheximide or sodium butyrate. When protein synthesis was completely inhibited by cycloheximide treatment, responsiveness to ACTH declined with a half-life of 20.5 h and responsiveness to PGE1 declined with a half-life of 75h. Because PGE1-stimulated cAMP production indicates intact adenylate cyclase catalytic activity, changes in ACTH-stimulated cAMP production appear to be due to specific changes in functional ACTH receptors.
D000311:Adrenal Glands / Q000166:cytology / Q000187:drug effects*; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology*; D000818:Animals; D002087:Butyrates / Q000494:pharmacology; D002417:Cattle; D002455:Cell Division / Q000187:drug effects; D000242:Cyclic AMP / Q000096:biosynthesis; D003513:Cycloheximide / Q000494:pharmacology; D003609:Dactinomycin / Q000494:pharmacology; D007700:Kinetics; D011458:Prostaglandins E / Q000494:pharmacology*; D014176:Protein Biosynthesis
D002087:Butyrates; D011458:Prostaglandins E; D003609:Dactinomycin; D000324:Adrenocorticotropic Hormone; D003513:Cycloheximide; D000242:Cyclic AMP