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Platelet and Vascular Prostaglandins in Uremia and Thrombotic Microangiopathy

  • Donatella Marchesi
  • Giuseppe Remuzzi

Abstract

A balance between vascular prostacyclin and platelet thromboxane has been proposed as a requisite for normal hemostatis. A derangment in such a balance would result in hemorrhage or thrombosis. Several factors regulate the interplay of prostacyclin and thromboxane. Albumin and haptoglobin inhibit prostaglandin (PG) synthesis, possibly acting on cyclooxygenase.1 On the other hand, bradykinin and angiotensin II stimulate arachidonic acid (AA) release from membrane phospholipids after binding to the cell surface.2,3 Thrombin is a potent stimulator of PGI2 synthesis by endothelial cells in culture,2,3 whereas β-thromboglobulin, a protein derived from platelet release reaction, reduces PGI2 generation4 after binding to a high-affinity receptor on cultured bovine endothelial cells.5

Keywords

Hemolytic Uremic Syndrome Thrombotic Thrombocytopenic Purpura Thrombotic Microangiopathy Uremic Patient Plasma Factor 
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

© Plenum Publishing Corporation 1983

Authors and Affiliations

  • Donatella Marchesi
    • 1
  • Giuseppe Remuzzi
    • 1
  1. 1.Division of Nephrology and DialysisOspedali Riuniti di BergamoBergamoItaly

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