Possible involvement of Ca2+-calmodulin system in cyclic AMP action in cholesterol ester hydrolytic response to ACTH in bovine adrenocortical cells.
In order to elucidate the relationship between cyclic AMP and the Ca2+-calmodulin system in the steroidogenic response to adrenocorticotropic hormone (ACTH), the effects of calmodulin inhibitors (trifluoperazine and W-7) on cortisol production and cellular cholesterol ester hydrolysis induced by ACTH or dibutyryl cyclic AMP in bovine adrenocortical cells were examined in the absence of extracellular Ca2+. These calmodulin inhibitors inhibited not only the cortisol production and the cholesterol ester hydrolysis induced by ACTH in the absence of extracellular Ca2+, but also inhibited the dibutyryl cyclic AMP-induced cortisol production and the cholesterol ester hydrolysis in the absence of extracellular Ca2+. These results suggested the possibility that cyclic AMP action was mediated by the Ca2+-calmodulin system in the activation process of cellular cholesterol ester hydrolysis in the steroidogenic response to ACTH.
D000302:Adrenal Cortex / Q000187:drug effects / Q000378:metabolism; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology*; D000818:Animals; D003994:Bucladesine / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D002147:Calmodulin / Q000037:antagonists & inhibitors / Q000378:metabolism*; D002417:Cattle; D002788:Cholesterol Esters / Q000378:metabolism*; D000242:Cyclic AMP / Q000378:metabolism*; D006854:Hydrocortisone / Q000096:biosynthesis; D006868:Hydrolysis; D066298:In Vitro Techniques
D002147:Calmodulin; D002788:Cholesterol Esters; D003994:Bucladesine; D000324:Adrenocorticotropic Hormone; D000242:Cyclic AMP; D002118:Calcium; D006854:Hydrocortisone