Skip to main content

Thank you for visiting You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Letter
  • Published:

Arterial dilations in response to calcitonin gene-related peptide involve activation of K+ channels


CALCITONIN gene-related peptide (CGRP) is a 37-amino-acid peptide produced by alternative processing of messenger RNA from the calcitonin gene1,2. CGRP is one of the most potent vasodilators known3. It occurs in and is released from perivascular nerves1,4 and has been detected in the blood stream5–7, suggesting that it is important in the control of blood flow8,9. The mechanism by which it dilates arteries is not known. Here, we report that arterial dilations in response to CGRP are partially reversed by blockers of the ATP-sensitive potassium channel (KATP), glibenclamide10–12 and barium10,13. We also show that CGRP hyperpolarizes arterial smooth muscle and that blockers of KATP channels reverse this hyperpolarization. Finally, we show that CGRP opens single K+ channels in patches on single smooth muscle cells from the same arteries. We propose that activation of KATP channels underlies a substantial part of the relaxation produced by CGRP.

This is a preview of subscription content, access via your institution

Access options

Buy this article

Prices may be subject to local taxes which are calculated during checkout

Similar content being viewed by others


  1. Rosenfeld, M. G. et al. Nature 304, 129–135 (1983).

    Article  ADS  CAS  Google Scholar 

  2. Emeson, R. B., Hedgiran, F., Yeakley, J. M., Guise, J. W. & Rosenfeld, M. G. Nature 341, 76–80 (1989).

    Article  ADS  CAS  Google Scholar 

  3. Brain, S. D., Williams, T. J., Tippins, J. R., Morris, H. R. & MacIntyre, I. Nature 313, 54–56 (1985).

    Article  ADS  CAS  Google Scholar 

  4. Mulderry, P. K. et al. Neuroscience 14, 947–954 (1985).

    Article  CAS  Google Scholar 

  5. Morris, H. R. et al. Nature 308, 746–748 (1984).

    Article  ADS  CAS  Google Scholar 

  6. Edbrooke, M. R. et al. EMBO J. 4, 715–724 (1985).

    Article  CAS  Google Scholar 

  7. McEwan, J. R. et al. Circulation 77, 1072–1080 (1988).

    Article  CAS  Google Scholar 

  8. Brain, S. D. & Williams, T. W. Nature 335, 73–75 (1988).

    Article  ADS  CAS  Google Scholar 

  9. Kawasaki, H., Tasaki, K., Saito, A. & Goto, K. Nature 335, 164–167 (1988).

    Article  ADS  CAS  Google Scholar 

  10. Standen, N. B. et al. Science 245, 177–180 (1989).

    Article  ADS  CAS  Google Scholar 

  11. Ashcroft, F. M. A. Rev. Neurosci. 11, 97–118 (1988).

    Article  CAS  Google Scholar 

  12. Stanfield, P. R. Trends Neurosci. 10, 335–339 (1987).

    Article  CAS  Google Scholar 

  13. Quayle, J. M., Standen, N. B. & Stanfield, P. R. J. Physiol. Lond. 405, 677–697 (1988).

    Article  Google Scholar 

  14. Quast, U. & Cook, N. S. Trends Pharmac. Sci. 10, 431–435 (1989).

    Article  CAS  Google Scholar 

  15. Saito, A., Masaki, T., Uchiyama, Y., Lee, T. J. F. & Goto, K. J. Pharmac. exp. Ther. 248, 455–462 (1989).

    CAS  Google Scholar 

  16. Miller, C., Moczydlowski, E., Latorre, R. & Phillips, M. Nature 313, 316–318 (1985).

    Article  ADS  CAS  Google Scholar 

  17. Villaroel, A., Alvarez, O., Oberhauser, A. & Latorre, R. Pflügers Arch. 413, 118–126 (1988).

    Article  Google Scholar 

  18. Huang, Y., Langton, P. D., Hescheler, J. K., Standen, N. B. & Nelson, M. T. Biophysical J. 57, 117a (1990).

    Article  ADS  Google Scholar 

  19. Nelson, M. T., Standen, N. B., Brayden, J. E. & Worley, J. F. Nature 336, 382–385 (1988).

    Article  ADS  CAS  Google Scholar 

  20. Dunne, M. J., Bullett, M. J., Li, G. D., Wollheim, C. B. & Petersen, O. H. EMBO J. 8, 413–420 (1989).

    Article  CAS  Google Scholar 

  21. Davies, N. W., Spruce, A. E., Standen, N. B. & Stanfield, P. R. J. Physiol. Lond. 413, 31–48 (1989).

    Article  CAS  Google Scholar 

  22. Spruce, A. E., Standen, N. B. & Stanfield, P. R. Nature 316, 736–738 (1985).

    Article  ADS  CAS  Google Scholar 

  23. Kakei, M., Noma, A. & Shibasaki, T. J. Physiol. Lond. 363, 441–462 (1985).

    Article  CAS  Google Scholar 

  24. Bevan, J. A. & Brayden, J. E. Circ. Res. 60, 309–326 (1985).

    Article  Google Scholar 

  25. Winquist, R. J. et al. J. Pharmac. exp. Ther. 248, 149–156 (1989).

    CAS  Google Scholar 

  26. Mulvany, M. & Halpern, W. Circ. Res. 41, 19–26 (1977).

    Article  CAS  Google Scholar 

  27. Colquhoun, D. in Microelectrode Techniques. The Plymouth Workshop Handbook. (eds Standen, N. B., Gray, P. T. A. & Whitaker, M. J.) 83–104 (Company of Biologists, Cambridge, 1987).

    Google Scholar 

  28. Hamill, O. P., Marty, A., Neher, E., Sakmann, B. & Sigworth, F. J. Pflügers Arch. 391, 85–100 (1981).

    Article  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations


Rights and permissions

Reprints and permissions

About this article

Cite this article

Nelson, M., Huang, Y., Brayden, J. et al. Arterial dilations in response to calcitonin gene-related peptide involve activation of K+ channels. Nature 344, 770–773 (1990).

Download citation

  • Received:

  • Accepted:

  • Issue Date:

  • DOI:

This article is cited by


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.


Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing