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Related Experiment Videos

Tetrandrine as a calcium antagonist

H Takemura1, K Imoto, H Ohshika

  • 1Department of Pharmacology, School of Medicine, Sapporo Medical University, Japan.

Clinical and Experimental Pharmacology & Physiology
|August 1, 1996
PubMed
Summary

Tetrandrine (TET) inhibits calcium (Ca2+) entry and release in various cells, but its effectiveness varies by cell type. This study investigated TET

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Area of Science:

  • Cellular Physiology
  • Pharmacology
  • Calcium Signaling

Background:

  • Calcium (Ca2+) mobilization is crucial for cellular functions.
  • Tetrandrine (TET) is known to affect Ca2+ signaling pathways.
  • Understanding TET's mechanism requires examining its effects on Ca2+ entry and release across different cell types.

Purpose of the Study:

  • To review the Ca2+ antagonism of tetrandrine (TET) on Ca2+ mobilization in various cell types.
  • To investigate the effects of TET on Ca2+ entry and release, particularly in response to agonists and thapsigargin (TG).
  • To determine if TET's action on Ca2+ signaling is cell-type dependent.

Main Methods:

  • Utilized inositol trisphosphate (IP3)-generating drugs and thapsigargin (TG) to stimulate Ca2+ mobilization.
  • Measured cytoplasmic Ca2+ concentrations ([Ca2+]i) in response to various stimuli in PC12, NIH/3T3, rat parotid acinar, Jurkat, and C6 cells.
  • Assessed the impact of TET on agonist- and TG-induced Ca2+ entry and IP3 production.

Main Results:

  • TET (100 µmol/L) inhibited high K+-induced Ca2+ increases in PC12 cells and partially inhibited bradykinin- or TG-induced Ca2+ entry.
  • In NIH/3T3 fibroblasts and rat parotid acinar cells, TET abolished Ca2+ entry induced by bombesin, carbachol, or TG.
  • TET did not inhibit Ca2+ entry in Jurkat cells but dose-dependently inhibited Ca2+ mobilization and IP3 production in C6 glioma cells, affecting both Ca2+ entry and release.

Conclusions:

  • Tetrandrine's (TET) effects on Ca2+ entry are cell-type specific.
  • TET can inhibit Ca2+ entry from extracellular sources and Ca2+ release from intracellular stores, as demonstrated in rat glioma C6 cells.
  • The findings highlight the complex role of TET in regulating cellular calcium homeostasis.

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