We examined the effect of the depletion of intracellular Ca 2+ stores on Ca 2+ influx in rat glomerulosa cells. Depletion of intracellular Ca 2+ stores was achieved by inhibiting sarco/endoplasmic reticulum-type Ca 2+ - ATPase with thapsigargin or 2,5-di-(t-butyl)-1,4-benzohydroquinone (t-BHQ). Both inhibitors induced a sustained rise in cytoplasmic Ca 2+ concentration. The initial rise was observed also in Ca 2+ -free medium, while the sustained phase disappeared, indicating that the latter requires Ca 2+ influx. In Ca 2+ -free medium, the readdition of Ca 2+ induced a steeper and higher rise in intracellular Ca 2+ concentration in thapsigargin-treated cells than in controls, supporting the role of Ca 2+ influx. In normal medium, the addition of Cd 2+ (80 μM) evoked an immediate inhibition of the sustained phase of thapsigargin response. The response to thapsigargin was insensitive to nifedipine. Thapsigargin failed to enhance Mn 2+ quenching of fura 2. Our results provide evidence for the existence of capacitative Ca 2+ influx in rat glomerulosa cells and indicate that dihydropyridine-sensitive Ca 2+ channels do not participate in capacitative Ca 2+ entry. High concentrations of thapsigargin and t-BHQ, similar to the reported effects of angiotensin II and vasopressin, inhibited K + -induced Ca 2+ signals. These effects appear, however, to be independent of the depletion of internal Ca 2+ stores.
|Original language||English (US)|
|Journal||American Journal of Physiology - Cell Physiology|
|Issue number||5 36-5|
|Publication status||Published - Jan 1 1994|
All Science Journal Classification (ASJC) codes
- Cell Biology