Inhibitory mechanisms of naloxone on human platelets

Joen Rong Sheu, Yen Mei Lee, Ling Wen Lee, Hsiang Ning Luk, Mao Hsiung Yen

Research output: Contribution to journalArticlepeer-review

4 Citations (Scopus)


1. In the present study, naloxone was tested for its antiplatelet activities in human platelet-rich plasma (PRP). In human PRP, naloxone (0.1-0.5 mmol/L) inhibited aggregation stimulated by a variety of agonists (i.e. collagen, adenosine diphosphate (ADP), U46619 and adrenaline). 2. Naloxone (0.1-0.5 mmol/L) did not significantly affect cyclic adenosine monophosphate and cGMP levels in human washed platelets, whereas naloxone (0.5 mmol/L) significantly inhibited thromboxane B2 formation stimulated by collagen (5 μg/mL) in human washed platelets. 3. Naloxone (0.5 mmol/L) significantly inhibited [3H]-inositol monophosphate formation of [3H]-myoinositol loaded platelets stimulated by collagen and U46619. Moreover naloxone did not influence the binding of 125I-triflavin to platelet membranes. Triflavin is an Arg-Gly-Asp-containing specific fibrinogen receptor antagonist. 4. Addition of naloxene (0.5 mmol/L) to platelet preparations tagged with diphenylhexatriene (DPH) resulted in a considerable decrease in relative fluorescence intensity. 5. It is suggested that the anti platelet effects of naloxone may be caused, at least partly, by the induction of conformational changes in the platelet membrane initially, followed by the inhibition of thromboxane A2 formation and phosphoinositide breakdown of platelets stimulated by agonists.

Original languageEnglish
Pages (from-to)585-591
Number of pages7
JournalClinical and Experimental Pharmacology and Physiology
Issue number7-8
Publication statusPublished - 1998


  • Inositol monophosphate
  • Membrane fluidity
  • Naloxone
  • Platelet aggregation

ASJC Scopus subject areas

  • Physiology (medical)
  • Physiology
  • Pharmacology


Dive into the research topics of 'Inhibitory mechanisms of naloxone on human platelets'. Together they form a unique fingerprint.

Cite this