We examined the effect of the depletion of intracellular Ca2+ stores on Ca2+ influx in rat glomerulosa cells. Depletion of intracellular Ca2+ stores was achieved by inhibiting sarco/endoplasmic reticulum-type Ca2+- ATPase with thapsigargin or 2,5-di-(t-butyl)-1,4-benzohydroquinone (t-BHQ). Both inhibitors induced a sustained rise in cytoplasmic Ca2+ concentration. The initial rise was observed also in Ca2+-free medium, while the sustained phase disappeared, indicating that the latter requires Ca2+ influx. In Ca2+-free medium, the readdition of Ca2+ induced a steeper and higher rise in intracellular Ca2+ concentration in thapsigargin-treated cells than in controls, supporting the role of Ca2+ influx. In normal medium, the addition of Cd2+ (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 Mn2+ quenching of fura 2. Our results provide evidence for the existence of capacitative Ca2+ influx in rat glomerulosa cells and indicate that dihydropyridine-sensitive Ca2+ channels do not participate in capacitative Ca2+ entry. High concentrations of thapsigargin and t-BHQ, similar to the reported effects of angiotensin II and vasopressin, inhibited K+-induced Ca2+ signals. These effects appear, however, to be independent of the depletion of internal Ca2+ stores.
|Journal||American Journal of Physiology - Cell Physiology|
|Issue number||5 36-5|
|Publication status||Published - Jan 1 1994|
- calcium channels
- manganese quench
ASJC Scopus subject areas
- Cell Biology