Capacitative Ca 2+ influx in adrenal glomerulosa cells: Possible role in angiotensin II response

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

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Abstract

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 languageEnglish (US)
JournalAmerican Journal of Physiology - Cell Physiology
Volume267
Issue number5 36-5
Publication statusPublished - Jan 1 1994
Externally publishedYes

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All Science Journal Classification (ASJC) codes

  • Physiology
  • Cell Biology

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