Haruhisa Nishi
Department of Pharmacology (I), Jikei University School of Medicine,
3 - 25 - 8, Nishi-Shinbashi, Minato-ku, Tokyo 105 - 8461, Japan
Abstract: 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 ƒÊg/ml) partially inhibited (approx. 55% inhibition)
extracellular ATP (100 ƒÊM)-induced steroidogenesis in BA cells. However,
PTX did not inhibit extracellular UTP (100 ƒÊM)-induced steroidogenesis.
Both ATP- and UTP-induced steroidogeneses were significantly inhibited by
suramin (50 - 200 ƒÊM). These effects were inhibited significantly by reactive
blue-2 (more than 100 ƒÊM) and pyridoxal-phosphate-6-azophenyl-2',4'-disulphonic
acid (more than 100 ƒÊM). Both nucleotides (1 - 100 ƒÊM) 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.
Keywords: Steroidogenesis, P2 receptor, Bovine adrenocortical cell, ATP,
UTP