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Involvement of Nitric Oxide on Calcium Mobilization and Arachidonic Acid Pathway Activation during Platelet

Debipriya Banerjee1, Sahana Mazumder1, Asru Kumar Sinha2

  • 1Department of Physiology, Rammohan College, University of Calcutta, Kolkata, India.

International Journal of Biomedical Science : IJBS
|April 30, 2016
PubMed

Insights

Platelet aggregation, crucial for blood clotting, is linked to acute coronary syndrome. This study reveals nitric oxide synthase inhibition triggers calcium release, promoting platelet aggregation and thromboxane A2 synthesis.

Area of Science:

  • Biochemistry
  • Hematology
  • Cardiovascular Research

Background:

  • Platelet aggregation is vital for hemostasis but its dysregulation contributes to acute coronary syndrome (ACS).
  • Thromboxane A2 (TXA2) synthesis, essential for platelet aggregation, requires arachidonic acid release, a mechanism not fully understood.
  • Nitric oxide (NO) is implicated in platelet function, but its role in arachidonic acid release remains unclear.

Purpose of the Study:

  • To investigate the role of nitric oxide (NO) in regulating arachidonic acid release from platelets.
  • To elucidate the signaling pathways involved in platelet aggregation induced by various agonists.
  • To determine the relationship between nitric oxide synthase (NOS) activity, calcium mobilization, and TXA2 production.

Main Methods:

  • Platelet-rich plasma (PRP) was treated with aggregating agents.
  • Cytosolic calcium ([Ca(2+)]) levels were measured using fluorescent spectroscopy (QUIN-2).
  • Nitric oxide (NO) was quantified via the methemoglobin method, arachidonic acid by HPLC, and TXA2 as ThromboxaneB2 (TXB2) by ELISA.

Main Results:

  • Aggregating agents inhibited NOS, decreasing NO production and increasing TXA2 synthesis.
  • Platelet activation led to a significant increase in cytosolic Ca(2+) levels.
  • Aspirin pre-treatment elevated platelet NO, suppressed Ca(2+) mobilization, and inhibited TXA2 synthesis.

Conclusions:

  • Platelet aggregation induced by agonists is mediated by cytosolic Ca(2+) mobilization.
  • The inhibition of nitric oxide synthase (NOS) plays a critical role in this calcium-dependent aggregation process.
  • Findings suggest a regulatory role for NO in preventing excessive platelet activation and TXA2 formation.

Keywords:
acute coronary syndromesarachidonic acidcalcium mobilizationnitric oxide

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