Two Different P2Y Receptors Linked to Steroidogenesis in Bovine Adrenocortical Cells

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Both extracellular adenosine 5′-triphosphate (ATP) and uridine 5′-triphosphate (UTP) induced corticoid production (steroidogenesis) concentration-dependently in bovine adrenocortical cells (BA cells). Pertussis toxin (PTX, approx. 2 μg/ml) partially inhibited (approx. 55% inhibition) extracellular ATP (100 μM)-induced steroidogenesis in BA cells. However, PTX did not inhibit extracellular UTP (100 μM)-induced steroidogenesis. Both ATP- and UTP-induced steroidogeneses were significantly inhibited by suramin (50 - 200 μM). These effects were inhibited significantly by reactive blue-2 (more than 100 μM) and pyridoxal-phosphate-6-azophenyl-2′, 4′-disulphonic acid (more than 100 μM). Both nucleotides (1 - 100 μM) induced inositol phosphates accumulation and intracellular Ca2+ mobilization, but PTX did not inhibit them. The RT-PCR procedure identified only P2Y2-receptor mRNA in BA cells. These results suggest that extracellular ATP induces steroidogenesis via a unique P2 receptor linked to PTX-sensitive guanine nucleotide-binding protein (G-protein), while extracellular UTP induces steroidogenesis via P2 receptor linked to PTX-insensitive G-protein. Thus, it was concluded that at least two different P2Y-like receptors linking to steroidogenesis exist in BA cells.
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