Capacitative Ca2+ influx in adrenal glomerulosa cells: Possible role in angiotensin II response

T. Rohacs, A. Bago, F. Deak, L. Hunyady, A. Spat

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41 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)C1246-C1252
JournalAmerican Journal of Physiology - Cell Physiology
Issue number5 36-5
StatePublished - 1994
Externally publishedYes


  • aldosterone
  • calcium channels
  • manganese quench
  • nifedipine
  • thapsigargin

ASJC Scopus subject areas

  • Physiology
  • Cell Biology


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