Angiotensin stimulation of adrenal fasciculata cells (original) (raw)

1988, Archives of biochemistry and …

In this paper we provide evidence to show that the pathways by which adrenocorticotropic hormone (ACTH) and angiotensin II (AII) stimulate steroidogenesis in bovine fasciculata cells are only partially independent. Both hormones have the same intrinsic activity but a 500-fold higher dose of AI1 is required to achieve 50% stimulation of steroidogenesis. Whereas ACTH acts by way of CAMP, AI1 appears to operate through protein kinase C. The phorbol ester, 12-O-tetradecanoylphorbol-13 acetate (TPA), and the calcium ionophore, A23187, each stimulate steroidogenesis and, when added together, act synergistically. To test the relationship between the ACTH and AI1 pathways, we added the two hormones simultaneously and measured steroid production. When the hormones were present at submaximal concentrations, their effects were additive. At maximal doses, steroid production was 40% above that elicited by either hormone alone. In contrast to the action of AI1 in the glomerulosa cell where it inhibits ACTH-stimulated CAMP formation, AI1 causes no inhibition in the fasciculata. Cycloheximide inhibits steroidogenesis stimulated by AI1 or a mixture of TPA and A23187. Scatchard analysis of the binding of '=I-AI1 to particulates from adrenal cortical fasciculata indicates the presence of a single class of binding sites (& = 0.6 X 10e8 M). Binding is not inhibited by ACTH. Biotin-containing AI1 analogs that bind specifically to the particulates have been evaluated as potential tools for avidin-biotin affinity chromatography of the receptor. One of these, [NL-6-(biotinylamido)hexyllys1,Va15] AII, is a promising candidate for receptor isolation. 8 1988AeademicPress,Ine.

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