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Morphine antagonises prostaglandin E1- mediated inhibition of human platelet aggregation

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Abstract

COLLIER and Roy1 have proposed that in morphine-sensitive neurones the receptor site may be adenyl cyclase, which is physiologically stimulated by prostaglandin E1 (PGE1) and pharmacologically blocked by opiates. An hypothesis has been put forward that morphine exerts its analgesic effect by inhibiting the stimulation by PGE1 of cyclic AMP formation in appropriate neurones2, whereas acute side effects of opiates may be caused by stimulation of prostaglandin biosynthesis3.

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Authors and Affiliations

  1. Departments of Pharmacology and Allergy, and Clinical Immunology, Copernicus Academy of Medicine in Cracow, 31–531 Cracow, 16, Grzegórzecka, Poland

    RYSZARD J. GRYGLEWSKI, ANDRZEJ SZCZEKLIK & KRZYSZTOF BIERON

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  1. RYSZARD J. GRYGLEWSKI
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  2. ANDRZEJ SZCZEKLIK
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  3. KRZYSZTOF BIERON
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GRYGLEWSKI, R., SZCZEKLIK, A. & BIERON, K. Morphine antagonises prostaglandin E1- mediated inhibition of human platelet aggregation. Nature 256, 56–57 (1975). https://doi.org/10.1038/256056a0

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