Steroidogenic action of calcium ions in isolated adrenocortical cells

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Abstract
The corticotropin[ACTH]-induced increase of total intracellular and receptor-bound cyclic[c]AMP in isolated rat adrenocortical cells was strictly dependent on extracellular Ca2+. A rise in bound cAMP with rising Ca2+ concentrations was accompanied by a decrease in free cAMP-receptor sites. A Ca2+-transport inhibitor abolished the rise in bound cAMP induced by corticotropin. During stimulation by corticotropin some Ca2+ has to be taken up in order to promote the rise of the relevant cAMP pool. Adenylate cyclase activity from isolated cells proved also to be dependent on a sub-millimolar Ca2+ concentration in the presence of corticotropin and GTP. When cells were treated under specific conditions, corticosterone production could be activated by Ca2+ in the absence of corticotropin (cells primed for Ca2+). Ca2+-induced steroidogenesis of these cells, in the absence of corticotropin, was also accompanied by an increase in total intracellular and receptor-bound cAMP, as was found previously with corticotropin-induced steroidogenesis in non-primed cells. Ca ionophores increasing the cell uptake of Ca2+ were not able to increase the cAMP pools in non-primed cells, unlike corticotropin in non-primed cells or Ca2+ in cells primed for Ca2+. During stimulation by either corticotropin or Ca2+ a possible cellular uptake of Ca2+ must be very limited and directed to a specific site which may affect the coupling of the hormone-receptor-adenylate cyclase complex.