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

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

Research output: Contribution to journalArticle

Abstract

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)
JournalAmerican Journal of Physiology - Cell Physiology
Volume267
Issue number5 36-5
StatePublished - Jan 1 1994
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Cell Biology
  • Clinical Biochemistry
  • Physiology

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