Effect of cyclandelate on prostacyclin release and cytosolic free calcium concentrations in human endothelial cells.
An increase in the concentration of cytosolic calcium plays a pivotal role in the stimulation of endothelial cells to release various mediators that are involved in vasodilatation and haemostasis. When these cells become damaged, a larger irreversible influx of calcium ions can cause 'calcium overload' and cell death. Cyclandelate may affect the influx of calcium ions in cells and act as a calcium overload blocker. Therefore, the effects of cyclandelate on prostacyclin (PGI2) release and cytosolic free calcium were investigated in cultured human endothelial cells. Cyclandelate did not inhibit the production of 6-keto-PGF1 alpha, a stable metabolite of prostacyclin. Similarly, cyclandelate (10(-6) to 10(-4) mol/L) and flunarizine (10(-6) to 10(-5) mol/L) had no effect on the increased concentrations of cytosolic free calcium in cells stimulated by bradykinin or thrombin, or on non-stimulated cells as evaluated with the calcium indicator fura-2. This was found both in serum-free conditions and in the presence of 10% human serum. It is likely that the rise in cytosolic free calcium concentration upon stimulation of cultured human endothelial cells depends on the influx of calcium ions from an intracellular storage pool.[1]References
- Effect of cyclandelate on prostacyclin release and cytosolic free calcium concentrations in human endothelial cells. van Hinsbergh, V.W. Drugs (1987) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
