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PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1987-9-25
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0012-6667
pubmed:author
pubmed:issnType
Print
pubmed:volume
33 Suppl 2
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
60-6
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1987
pubmed:articleTitle
Effect of cyclandelate on prostacyclin release and cytosolic free calcium concentrations in human endothelial cells.
pubmed:publicationType
Journal Article, In Vitro