Hydrogen peroxide activates NA+-dependent CA2+ influx in coronary endothelial cells

D. K. Bowles, W. F. Graier, Michael Sturek

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

The purpose of the present study was to examine the effect of short duration H2O2 exposure on coronary artery endothelial cell [Ca2+]i regulation. Freshly dispersed cells from porcine coronary artery were exposed to H2O2 (300 μmol/L) for 3 min while monitoring [Ca2+]i using fura-2 microfluorometry. H2O2 increased [Ca2+]i from 0.86 ± 0.03 to 2.19 ± 0.41 ratio units at 3 min of H2O2 (P <0.05). Intracellular Ca2+ remained elevated 3 min following removal of H2O2, yet H2O2 had no effect on the subsequent [Ca2+]i response to bradykinin (0.1 μmol/L). The H2O2-induced [Ca2+]i increase was completely abolished either by removal of extracellular Ca2+ or lowering extracellular Na+. Cells exposed to the Na+ ionophore, monensin, showed an increase in [Ca2+]i with a time course similar to that seen with H2O2. Furthermore, H2O2-induced Ca2+ influx was not attenuated by either Ni2+ (300 μmol/L) or econazole (10 μmol/L), excluding Ca2+ influx via the agonist-sensitive pathway. Thus, in coronary arterial endothelial cells, H2O2 increases Ca2+ influx in an extracellular Na+-dependent manner via an agonist-insensitive pathway.

Original languageEnglish (US)
Pages (from-to)1134-1139
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume287
Issue number5
DOIs
StatePublished - Oct 12 2001
Externally publishedYes

Fingerprint

Endothelial cells
Hydrogen Peroxide
Coronary Vessels
Endothelial Cells
Econazole
Cytophotometry
Monensin
Fura-2
Ionophores
Bradykinin
Swine
Monitoring

Keywords

  • Ca influx
  • Endothelium
  • Hydrogen peroxide
  • Intracellular Ca
  • Oxidative stress
  • Porcine

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

Hydrogen peroxide activates NA+-dependent CA2+ influx in coronary endothelial cells. / Bowles, D. K.; Graier, W. F.; Sturek, Michael.

In: Biochemical and Biophysical Research Communications, Vol. 287, No. 5, 12.10.2001, p. 1134-1139.

Research output: Contribution to journalArticle

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