Inhibitory mechanisms of naloxone on human platelets

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

研究成果: 雜誌貢獻文章同行評審

4 引文 斯高帕斯(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.

頁(從 - 到)585-591
期刊Clinical and Experimental Pharmacology and Physiology
出版狀態已發佈 - 1998

ASJC Scopus subject areas

  • 生理學
  • 藥學(醫學)
  • 藥理學、毒理學和藥劑學 (全部)


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