低温が副腎皮質コルチコイド産生に及ぼす抑制的影響

ウシ副腎皮質初代培養細胞を用いた検討

抄録

To explore the adrenocortical function at low temperatures, the time-dependent transition of corticoidogenesis (CG) as well as the effect of verapamil, a Ca²⁺ channel blocker, on CG were examined at 27°C using primary cultured bovine adrenocortical cells.
CG was induced using adrenocorticotropic hormone (ACTH, 10pM to 1μM), which stimulates the receptor-operated Ca²⁺ channel and adenylate cyclase activity; dibutyryl cyclic AMP (db-cAMP, 0.25 to 4mM), which mimics the intracellular action of cyclic AMP; and 30mM K⁺, which activates the voltage-dependent Ca²⁺ channel. Cells were incubated together with each of these secretaogues for 3 hours at 27°C.
Though the CG induced by 1nM ACTH-and 1mM db-cAMP increased for 3 hours at 27°C in the presence of 1.2mM Ca²⁺, the CG induced by 30mM K⁺ did not show any increase after 2 hours.
Both 5μM and 10μM of verapamil inhibited the CG induced by 10pM ACTH dose-dependently at 37°C. However, 5μM of verapamil showed no inhibiting effect at 27°C. Even 10μM verapamil did not influence the CG induced by 1mM db-cAMP.
In the absence of extracellular Ca²⁺, 10μM verapamil did not influence the CG induced by ACTH (10nM to 1μM) or db-cAMP (0.25 to 4mM) at 27°C.
These experiment results show that the functions of adrenocortical cells are kept effective for 3 hours and that Ca²⁺ is also important for CG at 27°C. Although it is well known that the increases in both cyclic AMP and intracellular Ca²⁺ are essential for the CG induced by various stimulants at 37°C, it is suggested that cyclic AMP plays a more important roll in CG than Ca²⁺ does at low temperatures.