Ca2+ influx is an important event associated with platelet activation and regulated by the content of intracellular Ca2+. Previous studies have suggested two different Ca2+ pools and two Ca2+ influx pathways exist in platelets. In the present study, we have investigated the regulation of thrombin- and thapsigargin-induced Ca2+ entry into human platelets, using fluorescent indicators to monitor Ca2+ mobilization and membrane potential. It was found that depletion of thapsigargin-sensitive Ca2+ stores was coupled to Ca2+ influx through a Ca2+-selective pathway. Additional release of Ca2+ from the thapsigargin-insensitive pool by thrombin caused the opening of a nonselective cation channel.

Keywords:
Thrombin, Thapsigargin, Inositol 1,4,5-trisphosphate, Cation channel, nonselective
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© 2000 National Science Council, ROC and S. Karger AG, Basel
2000
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