Extrusion mechanisms of intracellular Ca2+ in human aortic endothelial cells.
Although participation of the plasma membrane Ca2+ pump in Ca2+ efflux has been generally accepted, the existence of Na(2+)-Ca2+ exchange in endothelial cells is still controversial. In the present experiments, the role of Na(+)-Ca2+ exchange and Ca(2+)-ATPase were examined in cultured human aortic endothelial cells loaded with fura. In Ca(2+)-free solution, the declining phase of [Ca2+]i in response to histamine was clearly slowed with low Na+ solution or Ni2+. Vanadate also slightly slowed the declining phase. The declining phase was much more clearly slowed with La3+. The response to thapsigargin, a specific endoplasmic reticulum Ca2+ ATPase inhibitor, was much more clearly prolonged by those interventions. These results strongly imply the presence of Na(2+)-Ca2+ exchange and Ca2+ ATPase in the plasma membrane, and suggest that not only Ca2+ uptake into the internal stores but also Na(+)-Ca2+ exchange and plasma membrane Ca2+ ATPase have a physiological role in reducing [Ca2+]i elevated by receptor agonists and endoplasmic reticulum Ca(2+)-ATPase inhibitors in cultured human aortic endothelial cells.
Goto
Y
Y
Department of Pharmacology, Akita University School of Medicine, Japan.
Miura
M
M
Iijima
T
T
D001011:Aorta; D002118:Calcium / Q000378:metabolism*; D000252:Calcium-Transporting ATPases / Q000502:physiology*; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006801:Humans; D012964:Sodium / Q000378:metabolism*; D019284:Thapsigargin / Q000494:pharmacology; D014638:Vanadates / Q000494:pharmacology
D004791:Enzyme Inhibitors; D014638:Vanadates; D019284:Thapsigargin; D012964:Sodium; D000252:Calcium-Transporting ATPases; D002118:Calcium