Β2-adrenoceptor regulation of CGRP release from capsaicin-sensitive neurons

W. R. Bowles, C. M. Flores, D. L. Jackson, K. M. Hargreaves

Research output: Contribution to journalArticle

19 Scopus citations

Abstract

Previous studies have suggested that neurotransmitter substances from the sympatho-adrenomedullary system regulate pulpal blood flow (PBF), in part, by the inhibition of vasoactive neuropeptide release from pulpal sensory neurons. However, no study has evaluated the role of β-adrenoceptors. We evaluated the hypothesis that activation of β-adrenoceptors inhibits immunoreactive calcitonin gene-related peptide (iCGRP) release from capsaicin-sensitive nociceptive neurons via in vitro superfusion of bovine dental pulp. Either norepinephrine or epinephrine inhibited capsaicin-evoked iCGRP. The norepinephrine effect was blocked by the selective β2- adrenoceptor antagonist, ICI 118,551, but not by pre-treatment with the selective β1-adrenoceptor antagonist, atenolol. In addition, application of albuterol, a selective β2-adrenoceptor agonist, significantly blocked capsaicin-evoked release of iCGRP. Collectively, these studies demonstrate that activation of β2-adrenoceptors in dental pulp significantly reduces exocytosis of neuropeptides from capsaicin-sensitive nociceptors. This effect may have physiologic significance in regulating PBF. Moreover, since capsaicin selectively activates nociceptors, β2-adrenoceptor agonists may have clinical utility as peripherally acting therapeutics for dental pain and inflammation.

Original languageEnglish (US)
Pages (from-to)308-311
Number of pages4
JournalJournal of dental research
Volume82
Issue number4
DOIs
StatePublished - Apr 2003

Keywords

  • Albuterol
  • Atenolol
  • CGRP
  • Capsaicin
  • Dental pulp
  • Epinephrine
  • ICI 118,551
  • Norepinephrine
  • Superfusion

ASJC Scopus subject areas

  • Dentistry(all)

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