Capacitative Ca2+ entry into bovine adrenocortical fasciculata cells was investigated by using the mobilization of intracellular Ca2+ concentration ([Ca2+]i) and Ca2+-induced steroidogenesis as the indicators. Bovine adreno-cortical fasciculata cells on a glass coverslip were loaded with fura-2. The [Ca2+]i mobilization was detected by a change of fura-2 fluorescence intensity. In the intracellular Ca2+ store depleted cells, the addition of Ca2+ to the incubation medium elicited a marked and sustained increase in [Ca2+]i. In the intracellular Ca2+ store non-depleted cells, the addition of thapsigargin, an endoplasmic reticulum Ca2+-ATPase inhibitor, in the absence of extracellular Ca2+, induced a slight and transient increase in [Ca2+]i, but an extensive and sustained increase in [Ca2+]i was obtained by adding Ca2+ to the incubation medium after the thapsigargin treatment. The sustained increase induced by thapsigargin was not inhibited by nifedipine, but was inhibited by Zn2+ and Cd2+ in a concentration-dependent manner. The effect of Zn2+ was more potent than that of Cd2+. Thapsigargin stimulated steroidogenesis in the presence of extracellular Ca2+. The steroidogenic effect of thapsigargin was inhibited by Zn2+ and Cd2+ but not by nifedipine. These results suggest that there is, in bovine adrenocortical fasciculata cells, a steroidogenesis-linked Ca2+ entry process other than that involving voltage-operated Ca2+ channels and that the process might be capacitative Ca2+ entry.
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism