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Abstract

Platelet aggregation contributes to the pathogenesis of cardiovascular diseases. After activation it leads to dense granule secretion and 5-HT release. The question arises; how platelet aggregation is endogenously controlled during blood circulation. In preliminary studies, we observed that human plate-lets aggregate more rapidly when suspended in buffer as compared to those suspended in plasma (PRP). These observations point to the presence of an endogenous substance that may inhibit arachidonic acid– induced platelet aggregation. An analysis of plasma Cohn fractions demonstrated that most of the plasma inhibitory activity was associated with albumin–rich and α-globulin rich protein fractions. The identity of plasma endogenous inhibitors of platelet aggregation (EIPA) was established by affinity chromatography on Cibacron Blue F3G-A for specific removal of albumin. The association of α-globulins to EIPA activity was recognized as due to haptoglobin by affinity chromatography on a column of hemoglobin-sepharose. In addition, we also found that the distribution of EIPA activity varies according to sex and physiological state. These findings reveal that EIPA may act by modulation of arachidonic acid metabolism or seques-tering the fatty acid substrate.
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Authors and Affiliations

Nadia Khan
1 2 3
Magdalena Kurnik-Łucka
2
Gniewomir Latacz
3
Krzysztof Gil
2
Sheikh Arshad Saeed
1

  1. Dr. Panjwani Center for Molecular Medicine and Drug Research (PCMD), University of Karachi, Karachi, Pakistan
  2. Department of Pathophysiology, Faculty of Medicine, Jagiellonian University Medical College, Kraków, Poland
  3. Department of Technology & Biotechnology of Drugs, Faculty of Pharmacy, Jagiellonian University Medical College, Kraków, Poland

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