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Related Experiment Videos

Divalent cations effectively replace Ca2+ and support bradykinin induced noradrenaline release.

C Weiss1, D Sela, D Atlas

  • 1Department of Biological Chemistry, Hebrew University of Jerusalem, Israel.

Neuroscience Letters
|November 13, 1990
PubMed
Summary
This summary is machine-generated.

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Bradykinin (BK) triggers catecholamine release in PC-12 cells, dependent on extracellular cations like barium and strontium. This suggests BK utilizes a receptor-operated calcium channel for neurotransmitter secretion.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Pharmacology

Background:

  • Catecholamine secretion from pheochromocytoma cells (PC-12) can be induced by bradykinin (BK) or high KCl depolarization.
  • The precise mechanism of BK-induced catecholamine release, while known to be calcium-dependent, remains unclear.

Purpose of the Study:

  • To elucidate the mechanism of BK-induced catecholamine release in PC-12 cells.
  • To investigate the role of extracellular cations in supporting BK-mediated neurotransmitter release.

Main Methods:

  • PC-12 cells were stimulated with BK or high KCl in the presence of various extracellular cations (Ba2+, Sr2+, Ca2+, Mn2+, La3+).
  • BK-induced release of [3H]noradrenaline ([3H]NA) was quantified under different cation conditions.

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Main Results:

  • Extracellular cations differentially supported BK-induced [3H]NA release, with a rank order of potency: Ba2+ > Sr2+ > Ca2+ > Mn2+ ≈ La3+.
  • Barium (Ba2+) and strontium (Sr2+) supported significantly greater release than calcium (Ca2+), and this support was not saturable.
  • Lanthanum (La3+) and manganese (Mn2+) were less effective than Ca2+ in supporting release.

Conclusions:

  • Extracellular calcium (Ca2+) influx is essential for BK-induced catecholamine secretion.
  • Bradykinin (BK) likely mediates catecholamine release through a receptor-operated calcium channel (ROCC).