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ß₂-Adrenoceptor Regulation of CGRP Release from Capsaicin-sensitive Neurons

¹ Division of Endodontics, University of Minnesota School of Dentistry;
² Department of Endodontics, UTHSCSA School of Dentistry, Mail Code 7892, 7703 Floyd Curl Drive, San Antonio, TX 78229-3900; and
³ Department of Oral Medicine, University of Washington School of Dentistry;

*corresponding author, Hargreaves{at}UTHSCSA.edu

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 ß-adrenoceptors. We evaluated the hypothesis that activation of ß-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 ß₂-adrenoceptor antagonist, ICI 118,551, but not by pre-treatment with the selective ß₁-adrenoceptor antagonist, atenolol. In addition, application of albuterol, a selective ß₂-adrenoceptor agonist, significantly blocked capsaicin-evoked release of iCGRP. Collectively, these studies demonstrate that activation of ß₂-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, ß₂-adrenoceptor agonists may have clinical utility as peripherally acting therapeutics for dental pain and inflammation.

KEY WORDS: dental pulp • superfusion • CGRP • capsaicin • norepinephrine • albuterol • ICI 118 • 551 • atenolol • epinephrine

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