α‐Tocopherol and protein kinase C inhibition enhance platelet‐derived nitric oxide release

ABSTRACT Platelet activation is tightly regulated by products of the endothelium and platelets including nitric oxide (NO). Excess vascular oxidative stress has been associated with impaired NO release, and antioxidant status has been shown to alter endothelium‐derived NO bioactivity. Although physi...

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Veröffentlicht in:	The FASEB journal 2000-12, Vol.14 (15), p.2377-2379
Hauptverfasser:	Freedman, Jane E., Li, Liqing, Sauter, Ryan, Keaney, John F.
Format:	Artikel
Sprache:	eng
Schlagworte:	Alkaloids Animals antioxidant Antioxidants - pharmacology Benzophenanthridines blood platelet Enzyme Inhibitors - pharmacology Humans Mice Mice, Mutant Strains Models, Biological Nitric Oxide - metabolism Nitric Oxide Synthase - deficiency Nitric Oxide Synthase - metabolism Nitric Oxide Synthase Type II Nitric Oxide Synthase Type III Phenanthridines - pharmacology Phosphorylation Platelet Activation - drug effects Platelet Activation - physiology Platelet Aggregation Inhibitors - pharmacology Protein Kinase C - antagonists & inhibitors Superoxides - metabolism thrombosis vitamin E Vitamin E - pharmacology
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Zusammenfassung:	ABSTRACT Platelet activation is tightly regulated by products of the endothelium and platelets including nitric oxide (NO). Excess vascular oxidative stress has been associated with impaired NO release, and antioxidant status has been shown to alter endothelium‐derived NO bioactivity. Although physiological levels of α‐tocopherol are known to inhibit platelet function, the effect of α‐tocopherol on platelet NO release is unknown. Loading platelets with physiologic levels of α‐tocopherol increased platelet NO production ~1.5‐fold (P
ISSN:	0892-6638 1530-6860
DOI:	10.1096/fj.00-0360fje