Ca2+‐mediated ascorbate release from coronary artery endothelial cells
Journal Articles
Overview
Research
Identity
Additional Document Info
View All
Overview
abstract
The addition of Ca2+ ionophore A23187 or ATP to freshly isolated or cultured pig coronary artery endothelial cells (PCEC) potentiated the release of ascorbate (Asc). Cultured PCEC were used to characterize the Ca2+‐mediated release. An increase in Ca2+‐mediated Asc release was observed from PCEC preincubated with Asc, Asc‐2‐phosphate or dehydroascorbic acid (DHAA).The effects of various ATP analogs and inhibition by suramin were consistent with the ATP‐induced release being mediated by P2Y2‐like receptors.ATP‐stimulated Asc release was Ca2+‐mediated because (a) ATP analogs that increased Asc release also elevated cytosolic [Ca2+], (b) Ca2+ ionophore A23187 and cyclopiazonic acid stimulated the Asc release, (c) removing extracellular Ca2+ and chelating intracellular Ca2+inhibited the ATP‐induced release, and (d) inositol‐selective phospholipase C inhibitor U73122 also inhibited this release.Accumulation of Asc by PCEC was examined at Asc concentrations of 10 μM (Na+‐Asc symporter not saturated) and 5 mM (Na+‐Asc symporter saturated). At 10 μM Asc, A23187 and ATP caused an inhibition of Asc accumulation but at 5 mM Asc, both the agents caused a stimulation. Substituting gluconate for chloride did not affect the basal Asc uptake but it abolished the effects of A23187.PCEC but not pig coronary artery smooth muscle cells show a Ca2+‐ mediated Asc release pathway that may be activated by agents such as ATP.British Journal of Pharmacology (2006) 147, 131–139. doi:10.1038/sj.bjp.0706492
