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

Celeste Weiss, Dalit Sela, Daphne Atlas*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

19 Scopus citations

Abstract

Bradykinin (BK), a nonapeptide acting at the B2-type BK-receptor, and depolarization with high KCl (50 mM), induce catecholamine secretion in pheochromocytoma cells (PC-12). The mechanism underlying the BK-induced release, which is absolutely Ca2+-dependent, is not yet understood. Alkaline metals, barium (Ba2+), strontium (Sr2+) and other metal cations, manganese (Mn2+) or lanthanum (La3+), support BK-induced [3H]noradrenaline ([3H]NA) release. The extent of supporting transmitter release is dependent upon the specificity of the extracellular cation, with rank order potency of: Ba2+ > Sr2+ > Ca2+ > Mn2+La3+. The same rank order potency was observed for supporting both BK- and K+-induced release. [3H]NA release in the presence of Ba2+ or Sr2+ was much greater than in the presence of Ca2+, and unlike with Ca2+ was not saturable at the highest concentration measured. La3+ and Mn2+ were significantly less effective than Ca2+ at supporting release. These results strongly suggest that extracellular Ca2+ entry is essential for release, and that BK mediates release via a receptor-operated Ca2+ channel.

Original languageAmerican English
Pages (from-to)241-244
Number of pages4
JournalNeuroscience Letters
Volume119
Issue number2
DOIs
StatePublished - 13 Nov 1990

Keywords

  • Bradykinin
  • Depolarization
  • Exocytosis
  • Intracellular calcium
  • Noradrenaline
  • PC12 cell
  • Release

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