Letter | Published:

Do human platelets have opiate receptors?

Nature volume 288, pages 382383 (27 November 1980) | Download Citation

Subjects

Abstract

In their study of prostaglandin E1 (PGE1)-sensitive adenylate cyclase (AC) in rat brain homogenates, Collier and Roy1 claimed that the activity of this enzyme is inhibited by opiates. They also proposed that opiates exert their analgesic and allied effects by inhibiting AC of neurones that are normally stimulated by E prostaglandins2. Studies using neuroblastoma × glioma hybrid cells3,4 supported this hypothesis. However, subsequent studies with the mammalian brain5,6 and rat brain tissue slices7,8 yielded conflicting results. PGE1, also inhibits platelet aggregation9, probably through activation of platelet AC10. Gryglewski et al.11 showed that morphine inhibits the anti-aggregating effect of PGE1 on ADP- and adrenaline-induced platelet aggregation, and suggested that the inhibition by morphine is mediated through platelet AC activity. We report here our attempts to reproduce the results of Gryglewski et al. and our examination of the effect of morphine on PGE1-sensitive AC activity in platelet lysates and on PGE1-induced accumulation of cyclic AMP in intact platelets. The possible existence of opiate receptors in platelets was also assesed by direct binding studies with 3H-etorphine. In contrast to Gryglewski et al.11, we could not detect any effect of opiates on the aggregation of human platelets, nor did we find any other evidence supporting the presence of opiate receptors in these cells. Thus we conclude that the presence of opiate receptors in human platelets is unlikely.

Access optionsAccess options

Rent or Buy article

Get time limited or full article access on ReadCube.

from$8.99

All prices are NET prices.

References

  1. 1.

    & Nature 248, 24–27 (1974).

  2. 2.

    & Prostaglandins 7, 361–376 (1974).

  3. 3.

    , & Proc. natn. Acad. Sci. U.S.A. 72, 590–594 (1975).

  4. 4.

    , , & Nature 253, 120–122 (1975).

  5. 5.

    , & FEBS Lett. 51, 242–245 (1975).

  6. 6.

    , & Life Sci. 16, 1875–1876 (1976).

  7. 7.

    & Brain Res. 120, 263–268 (1977).

  8. 8.

    & Arch. Pharmac. 302, 103–106 (1978).

  9. 9.

    in Prostaglandins, Proc. 2nd Nobel Symp., Stockholm (eds Bergstrom, S. & Samuelson, B.) 241 (Interscience, New York, 1976).

  10. 10.

    & Biochem. biophys. Res. Commun. 35, 265–272 (1969).

  11. 11.

    , & Nature 256, 56–57 (1975).

  12. 12.

    & Br. J. Haemat. 26, 331–356 (1974).

  13. 13.

    Nature 194, 927–929 (1962).

  14. 14.

    , & J. Lab. clin. Med. 93, 638–644 (1979).

  15. 15.

    , & J. Cyclic Nucleotide Res. 2, 381–392 (1976).

  16. 16.

    & J. Anat. 96, 79–87 (1962).

  17. 17.

    Adv. Cyclic Nucleotide Res. 10, 35–55 (1979).

  18. 18.

    & FEBS Lett. 98, 44–48 (1979).

  19. 19.

    New Engl. J. Med. 286, 358–363 (1972).

  20. 20.

    , & Israel J. med. Sci. 14, 990 (1978).

  21. 21.

    , & Israel J. med. Sci. 15, 81 (1979).

  22. 22.

    , & Thromb. Res. 16, 107–116 (1979).

Download references

Author information

Affiliations

  1. Department of Neurology, Hadassah University Hospital, Jerusalem, Israel

    • A. Reches
  2. Department of Hematology, Hadassah University Hospital, Jerusalem, Israel

    • A. Eldor
  3. Department of Neurobiology, The Weizmann Institute of science, Rehovot, Israel 76100

    • Z. Vogel
  4. Department of Hormone research, The Weizmann Institute of science, Rehovot, Israel 76100

    • Y. Salomon

Authors

  1. Search for A. Reches in:

  2. Search for A. Eldor in:

  3. Search for Z. Vogel in:

  4. Search for Y. Salomon in:

About this article

Publication history

Received

Accepted

Published

DOI

https://doi.org/10.1038/288382a0

Comments

By submitting a comment you agree to abide by our Terms and Community Guidelines. If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate.