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Control of Ca2+ Mobilization and Polyphosphoinositide Metabolism in Platelets by Prostacyclin

  • George B. Zavoico
  • Stephen P. Halenda
  • David Chester
  • Maurice B. Feinstein
Part of the GWUMC Department of Biochemistry Annual Spring Symposia book series (GWUN)

Abstract

Cyclic AMP is perhaps the most important inhibitory regulator of platelet function. Dibutyryl cAMP, as well as agents that stimulate adenylate cyclase, can inhibit the characteristic responses of platelets to stimulation by agonists, i. e., shape change, aggregation and secretion, increased lipid metabolism, protein phosphorylation, and cytoskeleton assembly. Prostacyclin (PGI2) is the most potent physiological activator of platelet adenylate cyclase, and its role as a biological regulator of platelet function appears to be directly related to this action (Weksler, 1982). It has also been suggested that the antithrombotic effectiveness of certain agents observed clinically may be attributable to their antiphosphodiesterase activity, which enhances the action of prostacyclin, released from blood vessel walls, on platelet cAMP levels (Weksler, 1982).

Keywords

Adenylate Cyclase Human Platelet Myosin Light Chain Kinase Dibutyryl cAMP Stimulate Adenylate Cyclase 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media New York 1985

Authors and Affiliations

  • George B. Zavoico
    • 1
  • Stephen P. Halenda
    • 1
  • David Chester
    • 1
  • Maurice B. Feinstein
    • 1
  1. 1.Department of PharmacologyUniversity of Connecticut Health CenterFarmingtonUSA

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