A possible regulatory role of Ca++-calmodulin system in cellular cholesterol ester hydrolysis in the steroidogenic response to ACTH in bovine adrenocortical cells.

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Abstract
To corroborate the regulatory role of Ca2+-calmodulin system in the steroidogenic response to ACTH, the effects of calmodulin inhibitors (chlorpromazine, trifluoperazine and W-7 [N-(6-aminohexyl)-5-chloro-l-naphthalene sulfonamide]) on cortisol production and cellular cholesterol ester hydrolysis induced by ACTH in bovine adrenocortical cells were examined. Three calmodulin inhibitors diminished not only the cholesterol ester hydrolysis and cortisol production induced by ACTH in the presence of Ca2+, but also inhibited the Ca2+-induced hydrolysis and cortisol production in the absence of ACTH. Neither cortisol production in crude mitochondrial fraction nor the ACTH-induced Ca2+-influx was affected by chlorpromazine. The Ca2+-calmodulin system apparently plays a significant regulatory role in the supply of free cholesterol to the adrenal mitochondria in the steroidogenic response to ACTH.

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