Display options
Cite
Stubbs CM, Waldron GJ, Connor HE, et al. Characterization of the receptor mediating relaxation to substance P in canine middle cerebral artery: no evidence for involvement of substance P in neurogenically mediated relaxation. Br J Pharmacol. 1992;105(4):875-80doi: 10.1111/j.1476-5381.1992.tb09071.x.
Stubbs, C. M., Waldron, G. J., Connor, H. E., & Feniuk, W. (1992). Characterization of the receptor mediating relaxation to substance P in canine middle cerebral artery: no evidence for involvement of substance P in neurogenically mediated relaxation. British journal of pharmacology, 105(4), 875-80. https://doi.org/10.1111/j.1476-5381.1992.tb09071.x
Stubbs, C M, et al. "Characterization of the receptor mediating relaxation to substance P in canine middle cerebral artery: no evidence for involvement of substance P in neurogenically mediated relaxation." British journal of pharmacology vol. 105,4 (1992): 875-80. doi: https://doi.org/10.1111/j.1476-5381.1992.tb09071.x
Stubbs CM, Waldron GJ, Connor HE, Feniuk W. Characterization of the receptor mediating relaxation to substance P in canine middle cerebral artery: no evidence for involvement of substance P in neurogenically mediated relaxation. Br J Pharmacol. 1992 Apr;105(4):875-80. doi: 10.1111/j.1476-5381.1992.tb09071.x. PMID: 1380374; PMCID: PMC1908684.
Copy Download .nbib Format: NLM
Share it on
Full text links
Wiley Free PMC Article

Br J Pharmacol. 1992 Apr;105(4):875-80. doi: 10.1111/j.1476-5381.1992.tb09071.x.

Characterization of the receptor mediating relaxation to substance P in canine middle cerebral artery: no evidence for involvement of substance P in neurogenically mediated relaxation.

British journal of pharmacology

C M Stubbs, G J Waldron, H E Connor, W Feniuk

Affiliations

  1. Department of Neuropharmacology, Glaxo Group Research, Ware, Herts.

PMID: 1380374 PMCID: PMC1908684 DOI: 10.1111/j.1476-5381.1992.tb09071.x
Free PMC Article

Abstract

1. The aim of this study was to characterize the neurokinin receptor which mediates relaxation of dog isolated middle cerebral artery by the use of selective agonists and antagonists and to establish whether substance P is involved in the neurogenically mediated relaxant response in this vessel. 2. Substance P caused concentration-related, endothelium-dependent relaxations of dog isolated middle cerebral artery, contracted with prostaglandin F2 alpha. The selective NK1 receptor agonists, GR73632 and substance P methyl ester (SPOMe), also caused relaxation with similar maximum effects to those of substance P. GR73632 and SPOMe were approximately 20 times and 6 times less potent respectively than substance P. The selective NK2 and NK3 receptor agonists, GR64349 and senktide, were only weakly active in causing relaxation being at least 425 times and 245 times less potent respectively than substance P. 3. The selective NK1 receptor antagonist, GR82334, was a potent, specific, competitive antagonist of the relaxant effects of substance P. In contrast, the selective NK2 receptor antagonist, R396 (10 microM) had no effect on the response to substance P. 4. Electrical field stimulation of dog isolated middle cerebral artery, contracted with prostaglandin F2 alpha, caused neurogenically mediated, non-adrenergic non-cholinergic (NANC) relaxations. These NANC relaxations were unaffected by endothelium removal, GR82334 (10 microM) or by capsaicin (10 microM) treatment. However, the nitric oxide synthesis inhibitor, L-NG-monomethyl arginine methyl ester (L-NMMA) (100 microM) markedly attenuated the response to electrical stimulation. 5. These results suggest that substance P causes relaxation of dog isolated middle cerebral artery via activation of NK1 receptors. However, substance P does not appear to be involved in NANC neurotransmission. In contrast, the marked inhibitory effect of L-NMMA on NANC relaxations implicates nitric oxide in NANC neurotransmission in this vessel.

References

  1. Br J Pharmacol. 1990 Jul;100(3):589-92 - PubMed
  2. Eur J Pharmacol. 1990 Apr 25;179(3):457-62 - PubMed
  3. Neurosci Lett. 1985 Nov 20;62(1):131-6 - PubMed
  4. Naunyn Schmiedebergs Arch Pharmacol. 1986 May;333(1):59-64 - PubMed
  5. J Cardiovasc Pharmacol. 1987 Dec;10(6):675-82 - PubMed
  6. Br J Pharmacol. 1989 Nov;98(3):717-20 - PubMed
  7. Pharmacology. 1989;38(1):1-15 - PubMed
  8. Biochem Pharmacol. 1989 Jun 1;38(11):1709-15 - PubMed
  9. J Pharmacol Exp Ther. 1989 Jan;248(1):455-62 - PubMed
  10. Trends Pharmacol Sci. 1988 Aug;9(8):290-5 - PubMed
  11. Z Zellforsch Mikrosk Anat. 1972;134(3):311-25 - PubMed
  12. Am J Physiol. 1982 Aug;243(2):H145-53 - PubMed
  13. Jpn J Pharmacol. 1981 Dec;31(6):1071-9 - PubMed
  14. Brain Res. 1982 Aug 5;245(1):171-4 - PubMed
  15. Science. 1984 May 25;224(4651):898-901 - PubMed
  16. Circ Res. 1978 Apr;42(4):535-42 - PubMed
  17. Br J Pharmacol. 1990 Apr;99(4):767-73 - PubMed
  18. Biochem Biophys Res Commun. 1990 Jul 16;170(1):308-13 - PubMed
  19. Br J Pharmacol. 1990 Aug;100(4):749-52 - PubMed
  20. Neurosci Lett. 1986 Jan 30;63(3):310-4 - PubMed
  21. EMBO J. 1986 Nov;5(11):2805-8 - PubMed
  22. Br J Pharmacol. 1989 Jan;96(1):170-8 - PubMed
  23. Clin Exp Pharmacol Physiol. 1989 Dec;16(12):933-8 - PubMed
  24. Cerebrovasc Brain Metab Rev. 1989 Fall;1(3):230-52 - PubMed
  25. Nature. 1987 Jun 11-17;327(6122):524-6 - PubMed
  26. Brain Res. 1967 Dec;6(4):773-6 - PubMed
  27. Neuroscience. 1982 Feb;7(2):447-59 - PubMed
  28. Eur J Pharmacol. 1983 Jan 28;87(1):77-84 - PubMed
  29. Br J Pharmacol Chemother. 1959 Mar;14(1):48-58 - PubMed
  30. Br J Pharmacol. 1976 Oct;58(2):211-21 - PubMed
  31. Br J Pharmacol. 1991 Mar;102(3):567-72 - PubMed
  32. Br J Pharmacol. 1991 Sep;104(1):91-6 - PubMed
  33. Br J Pharmacol. 1990 Aug;100(4):663-4 - PubMed

Substances

MeSH terms

Publication Types

LinkOut - more resources