Potentiation by adrenaline of Ca2+ influx and mobilization in stimulated human platelets: dissociation from thromboxane generation and aggregation

Thromb Haemost. 1988 Apr 8;59(2):212-5.

Abstract

In a medium containing 1 mM extracellular Ca2+ (Ca2+o), the prior addition of 0.5 microM adrenaline to quin 2-loaded human platelets increased both the rate and amplitude of the rise in cytosolic free Ca2+ (Ca2+i) in response to sub-threshold concentrations of thrombin and PAF and these effects were not prevented by blocking either fibrinogen binding and aggregation or cyclo-oxygenase. In the presence of 2 mM EGTA [( Ca2+o] less than 100 nM), the rate, but not the extent of rise of [Ca2+i] was enhanced by adrenaline, and this was also unaffected by blockade of cyclo-oxygenase. Addition of adrenaline 1 min after the other agonist in the presence of 1 mM Ca2+o resulted in aggregation without further elevation of [Ca2+i]. Adrenaline thus enhances both influx and intracellular mobilization of Ca2+ by a mechanism independent of both fibrinogen binding and thromboxane production, but these effects do not fully explain its potentiation of aggregation by other agonists.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Blood Platelets / drug effects*
  • Blood Platelets / metabolism
  • Calcium / blood*
  • Drug Synergism
  • Epinephrine / pharmacology*
  • Humans
  • In Vitro Techniques
  • Platelet Activating Factor
  • Platelet Aggregation / drug effects
  • Thrombin / pharmacology
  • Thromboxanes / blood

Substances

  • Platelet Activating Factor
  • Thromboxanes
  • Thrombin
  • Calcium
  • Epinephrine