Why the study?
Do agonists stimulate bivalent-cation influx into human endothelial cells?
Do agonists stimulate bivalent-cation influx into human endothelial cells?
Agonists such as thrombin and histamine stimulate the influx of bivalent cations into human endothelial cells, a process that follows intracellular calcium release and is independent of elevated cytoplasmic calcium levels.
May inform endothelial Ca2+ signaling mechanisms; leaves open translation to human cells and clinical relevance.
Human umbilical-vein endothelial cells stimulated with thrombin or histamine show an increase in [Ca2+]i (cytoplasmic free calcium concn.) that is maintained well above the basal pre-stimulated value as long as agonist and a source of extracellular Ca2+ are present. These results provide circumstantial evidence that agonists stimulate influx of Ca2+ across the plasma membrane and into the cytoplasm. Here, we have used Mn2+ as the extracellular bivalent cation which can bind to the fluorescent Ca2+ indicator fura-2 to quench its fluorescence completely. Human umbilical-vein endothelial cells were loaded with fura-2 and, in the presence of extracellular Mn2+, thrombin and histamine were shown to cause quenching of the intracellular dye. This result demonstrates conclusively that agonists can stimulate the influx of bivalent cations. Stimulated discharge of Ca2+ from intracellular stores and influx of Mn2+ were temporally resolved in the same cells to show that release of Ca2+ from intracellular stores clearly precedes influx. Influx of Mn2+ was also demonstrated when extracellular Mn2+ was added after agonist at a time when [Ca2+]i had fallen back to the basal value, showing that influx is not dependent on elevated [Ca2+]i.
No takes yet. Share an insight, caveat, or question.
Hallam et al. (1988) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: