Kinetics of store-operated Ca2+ influx evoked by endomembrane Ca2+-ATPase inhibitors in human platelets.

  title={Kinetics of store-operated Ca2+ influx evoked by endomembrane Ca2+-ATPase inhibitors in human platelets.},
  author={Wim M. J. Vuist and Marion A. H. Feijge and Johan W. M. Heemskerk},
  journal={Prostaglandins, leukotrienes, and essential fatty acids},
  volume={57 4-5},
1 Citations
Calcium and Platelets
Intervention studies show that in particular antiplatelet drugs provide a risk reduction of one out of every four cases of coronary and cerebral artery diseases.


Indirect regulation of Ca2+ entry by cAMP-dependent and cGMP-dependent protein kinases and phospholipase C in rat platelets.
Ca2+ entry in rat platelets is mostly secondary to store depletion, is not directly downregulated by cAMP-dependent and cGMP-dependent protein kinase, but indirectly by inhibition of store depletion and is stimulated by increased mobilisation of Ca2+ from the stores.
Ca2+ release from platelet intracellular stores by thapsigargin and 2,5-di-(t-butyl)-1,4-benzohydroquinone: relationship to Ca2+ pools and relevance in platelet activation.
Tg and tBuBHQ are effective in releasing the Ins(1,4,5)P3-sensitive Ca2+ pool in platelets, indicating agonist utilization of a Ca(2+)-ATPase inhibitor-insensitive pool.
Store-activated Ca2+ inflow in Xenopus laevis oocytes: inhibition by primaquine and evaluation of the role of membrane fusion.
It is concluded that membrane fusion processes are unlikely to be involved in the link between the release of Ca2+ from the endoplasmic reticulum and activation of SACCs.
Thapsigargin-induced Calcium Influx in the Absence of Detectable Tyrosine Phosphorylation in Human Platelets*
Thapsigargin-induced SOC influx can occur without detectable tyrosine phosphorylation and the inhibition of SOC influx by tyrosin kinase inhibitors does not correlate with their ability to prevent tyrosines phosphorylated.
Different effects of endothelin‐3 on the Ca2+ discharge induced by agonists and Ca2+‐ATPase inhibitors in human platelets
The small but significant inhibitory effect of ET‐3 leads to propose that endothelin‐3 acts as a modulator of platelet activation in Ca2+ mobilization from an internal pool dependent on the stimulation of thrombin and thromboxane A2 receptors and insensitive to the direct effect of Ca2-ATPase inhibitors.
Primaquine, an inhibitor of vesicular transport, blocks the calcium-release-activated current in rat megakaryocytes.
Evidence is provided that the channels carrying Icrac may be stored in a vesicular membrane compartment and transferred to the plasma membrane following store depletion, as well as the recognized role of GTPases in the regulation of vesicle trafficking.