Abstract
Administration of aspirin (81 mg/day for 2-3 weeks) in nine healthy volunteers (out of an initial ten subjects, only nine qualified) resulted in a greater than 95% decrease of thromboxane B2 production by thrombin-stimulated platelets. At the same time, ligand binding studies with a thromboxane A2 antagonist, 125I-PTA-OH, measurements of shape change, and aggregation of platelets stimulated with U46619, a prostaglandin H2 analogue, indicated that administration of aspirin to normal human subjects does not result in the up-regulation of platelet thromboxane A2/prostaglandin H2 receptors.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adult
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Aspirin / administration & dosage
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Aspirin / pharmacology*
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Blood Platelets / drug effects*
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Blood Platelets / metabolism
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Female
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Humans
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Male
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Platelet Aggregation / drug effects
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Prostaglandin Endoperoxides, Synthetic / pharmacology
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Receptors, Prostaglandin / metabolism*
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Receptors, Thromboxane
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Receptors, Thromboxane A2, Prostaglandin H2
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Thrombin
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Thromboxane A2 / analogs & derivatives
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Thromboxane A2 / antagonists & inhibitors
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Thromboxane A2 / pharmacology
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Thromboxane B2 / metabolism
Substances
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Prostaglandin Endoperoxides, Synthetic
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Receptors, Prostaglandin
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Receptors, Thromboxane
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Receptors, Thromboxane A2, Prostaglandin H2
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Thromboxane B2
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Thromboxane A2
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I-PTA-OH
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Thrombin
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Aspirin