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INHIBITORY MECHANISMS OF NALOXONE ON HUMAN PLATELETS
Author(s) -
Sheu JoenRong,
Lee YenMei,
Lee LingWen,
Luk HsiangNing,
Yen MaoHsiung
Publication year - 1998
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1998.tb02256.x
Subject(s) - (+) naloxone , platelet , inhibitory postsynaptic potential , pharmacology , psychology , neuroscience , anesthesia , medicine , opioid , receptor
SUMMARY 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 [ 3 H]‐inositol monophosphate formation of [ 3 H]‐myoinositol‐loaded platelets stimulated by collagen and U46619. Moreover, naloxone did not influence the binding of 125 I‐triflavin to platelet membranes. Triflavin is an Arg‐Gly‐Asp‐containing specific fibrinogen receptor antagonist. 4. Addition of naloxone (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 A 2 formation and phosphoinositide breakdown of platelets stimulated by agonists.