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.