Calcium ion as "second messenger" in corticoidogenic action of ACTH.
The correlation between corticoidogenesis and Ca2+-influx in the cell was investigated using isolated rat or bovine adrenocortical cells. 1) ACTH-induced corticoidogenesis in both rat and bovine adrenocortical cells was enhanced in parallel with increasing concentration of external Ca2+. In the bovine cells but not in the rat cells, moreover, the marked stimulatory effect of external Ca2+ on the corticoidogenesis was observed despite the absence of ACTH. 2) Ca2+-influx and corticoidogenesis always occurred unitedly. 3) Verapamil markedly inhibited either corticoidogenesis or Ca2+-influx in response to ACTH. 4) The stimulatory effect of Ca2+ on corticoidogenesis was completely blocked by cycloheximide. It was therefore suggested that Ca2+ could regulate corticoidogenesis as a primary "second messenger" of ACTH through biosynthesis of so-called steroidogenic protein.
D000302:Adrenal Cortex / Q000187:drug effects / Q000502:physiology*; D000305:Adrenal Cortex Hormones / Q000096:biosynthesis*; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology* / Q000502:physiology; D000818:Animals; D002118:Calcium / Q000494:pharmacology* / Q000502:physiology; D002417:Cattle; D000242:Cyclic AMP / Q000502:physiology; D003513:Cycloheximide / Q000494:pharmacology; D005260:Female; D051381:Rats; D014700:Verapamil / Q000494:pharmacology
D000305:Adrenal Cortex Hormones; D000324:Adrenocorticotropic Hormone; D003513:Cycloheximide; D014700:Verapamil; D000242:Cyclic AMP; D002118:Calcium