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Effects of sodium removal on calcium mobilization and dense granule secretion induced by thrombin in human platelets

M T Alonso1, A Sanchez, J García-Sancho

  • 1Departamento de Bioquímica y Biología Molecular y Fisiología, Facultad de Medicina, Universidad de Valladolid, Spain.

Biochimica Et Biophysica Acta
|June 6, 1989
PubMed

Insights

Extracellular sodium is crucial for thrombin-induced calcium release from intracellular stores in human platelets, impacting ATP and serotonin secretion. Sodium removal impairs this calcium mobilization and subsequent dense granule secretion.

Area of Science:

  • Biochemistry
  • Hematology
  • Cell Physiology

Background:

  • Platelet activation involves calcium mobilization from intracellular stores.
  • Extracellular ions play a role in regulating platelet function.

Purpose of the Study:

  • To investigate the role of extracellular sodium in thrombin-induced calcium mobilization and dense granule secretion in human platelets.
  • To determine if sodium is essential for calcium release from intracellular stores.

Main Methods:

  • Human platelets were treated with aspirin.
  • Extracellular sodium was removed.
  • Calcium mobilization was measured using intracellular calcium indicators.
  • ATP and serotonin secretion were quantified.
  • Platelet activation was induced by thrombin and ionomycin.

Main Results:

  • Removal of extracellular sodium significantly decreased thrombin-induced calcium mobilization from intracellular stores.
  • ATP and serotonin secretion were reduced in the absence of extracellular sodium.
  • Calcium mobilization induced by ionomycin was not affected by sodium removal.
  • Secretion correlated positively with intracellular calcium levels, but sodium absence altered the relationship.

Conclusions:

  • Extracellular sodium is required for normal thrombin-induced calcium release from intracellular stores.
  • Sodium is essential for dense granule secretion in response to thrombin.
  • Platelet secretion involves calcium-dependent and calcium-independent pathways.

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