Skip to main content
Log in

Proadrenomedullin N-terminal 20 peptide inhibits adrenocorticotropin secretion from cultured pituitary cells, possibly via activation of a potassium channel

  • Published:
Endocrine Aims and scope Submit manuscript

Abstract

Preproadrenomedullin is processed into at least two biologically active peptides, adrenomedullin (AM) and proadrenomedullin N-terminal 20 peptide (PAMP). Both peptides are hypotensive; however, they exert this action via differing mechanisms. In pituitary cells in culture, both basal and releasing factor-stimulated adrenocorticotropin (ACTH) secretion is inhibited by AM. Here we report that basal, but not stimulated, ACTH secretion from cultured rat pituitary cells is also inhibited by PAMP. The effect is dose-related, occurs in a physiologically relevant dose range that is similar to that of AM, and is blocked by the potassium channel blocker, glybenclamide. The failure of glybenclamide to inhibit AM’s effects on ACTH secretion indicates that in pituitary, as in other tissues, these two products of the same prohormone can exert similar biologic activity, although via differing mechanisms.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Similar content being viewed by others

References

  1. Kitamura, K., Sakata, J., Kangawa, K., Kojima, H., Matsuo, H., and Eto, T. (1993). Biochem. Biophys. Res. Commun. 194, 720–725.

    Article  PubMed  CAS  Google Scholar 

  2. Ishimitsu, T., Kojima, M., Hino, J., Matsuoka, H., Kitamura, K., Eto, T., et al. (1994). Biochem. Biophys. Res. Commun. 203, 631–639.

    Article  PubMed  CAS  Google Scholar 

  3. Feng, C. J., Kang, B., Kaye, A. D., Kadowitz, P. J., and Nossman, B. D. (1994). Life Sci. 55, 433–438.

    Article  Google Scholar 

  4. Hirata, Y., Hayakawa, H., Suzuki, Y., Suzuki, Y., Ikenouchi, H., Kohmoto, O., Kimura, K., et al. (1995). Hypertension 25, 790–795.

    PubMed  CAS  Google Scholar 

  5. Shimosawa, T., Ito, Y., Ando, K., Kitamura, K., Kangawa, K., and Fujita, T. (1995). J. Clin. Invest. 96, 1672–1676.

    PubMed  CAS  Google Scholar 

  6. Andreis, P. G., Neri, G., Prayer-Galetti, T., Rossi, G. P., Gottardo, G., Malendowicz, L. K., et al. (1997). J. Clin. Endocrinol. Metab. 82, 1167–1170.

    Article  PubMed  CAS  Google Scholar 

  7. Andreis, P. G., Mazzocchi, G., Rebuffat, P., and Nussdorfer, G. G. (1997). Life Sci. 60, 1693–1697.

    Article  PubMed  CAS  Google Scholar 

  8. Yamaguchi, T., Baba, K., Doi, Y., Yano, K., Kitamura, K., and Eto, T. (1996). Hypertension 28, 308–314.

    PubMed  CAS  Google Scholar 

  9. Ebara, T., Mura, K., Okumura, M., Matsuura, T., Kim, S., Yukimura, T., et al. (1994) Eur. J. Pharmacol. 263, 69–73.

    Article  PubMed  CAS  Google Scholar 

  10. Murphy, T. C. and Samson, W. K. (1995). Endocrinology 136, 2459–2463.

    Article  PubMed  CAS  Google Scholar 

  11. Samson, W. K. and Murphy, T. C. (1996). Endocrinology 138, 613–616.

    Article  Google Scholar 

  12. Katoh, F., Kitamura, K., Niina, H., Yamamoto, R., Washimine, H., Kangawa, K., et al. (1995). J. Neurochem. 64, 459–461.

    Article  PubMed  CAS  Google Scholar 

  13. Takano, K., Yamashita, N., and Fujita, T. (1996). J. Clin. Invest. 98, 14–17.

    Article  PubMed  CAS  Google Scholar 

  14. Samson, W. K., Murphy, T. C., and Schell, D. A. (1995). Endocrinology 136, 2349–2352.

    Article  PubMed  CAS  Google Scholar 

  15. Kapas, S., Catt, K. J., and Clark, A. J. L. (1995). J. Biol. Chem. 270, 25,344–25,347.

    CAS  Google Scholar 

  16. Takahashi, K., Satoh, F., Sone, M., Murakami, O., Sasano, H., Mouri, T., et al. (1997). Peptides 18, 1051–1053.

    Article  PubMed  CAS  Google Scholar 

  17. Sakata, J., Shimokubo, T., Kitamura, K., Nakamura, S., Kangawa, K., Matsuo, H., et al. (1994). FEBS Lett. 352, 105–108.

    Article  PubMed  CAS  Google Scholar 

  18. Wang, X. and Greer, M. A. (1994). Mol. Cell. Endocrinol. 109, 11–18.

    Article  Google Scholar 

  19. Lang, M. G., Paterno, R., Faraci, F. M., and Heistad, D. D. (1997). Stroke 28, 181–185.

    PubMed  CAS  Google Scholar 

  20. Quast, U. and Cook, N. S. (1989). J. Pharmacol. Exp. Ther. 250, 261–271.

    PubMed  CAS  Google Scholar 

  21. Parkes, D. G. and May, C. N. (1995). J. Neuroendocrinol. 7, 923–929.

    Article  PubMed  CAS  Google Scholar 

  22. Karschin, C., Schreibmayer, W., Dascal, N., Lester, H., Davidson, N., and Karschin, A. (1994). FEBS Lett. 348, 139–144.

    Article  PubMed  CAS  Google Scholar 

  23. Wang, X., Inukai, T., Greer, M. A., and Greer, S. E. (1994). Brain Res. 662, 83–87.

    Article  PubMed  CAS  Google Scholar 

  24. Samson, W. K. (1997). In: Endocrinology, Basic and Clinical Principles, Conn, P. M. and Melmed, S. (eds.). Humana Press: Totowa, NJ.

    Google Scholar 

  25. Samson, W. K., Said, S. I., Snyder, G. D., and McCann, S. M. (1979). Peptides 1, 325–332.

    Article  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Willis K. Samson.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Samson, W.K., Murphy, T.C. & Resch, Z.T. Proadrenomedullin N-terminal 20 peptide inhibits adrenocorticotropin secretion from cultured pituitary cells, possibly via activation of a potassium channel. Endocr 9, 269–272 (1998). https://doi.org/10.1385/ENDO:9:3:269

Download citation

  • Received:

  • Revised:

  • Accepted:

  • Issue Date:

  • DOI: https://doi.org/10.1385/ENDO:9:3:269

Key Words

Navigation