Prostaglandin E-2 enhances bradykinin-evoked iCGRP release in bovine dental pulp

Mediators produced during inflammation are responsible for hyperalgesia and expression of neurotransmitters and receptors in the nervous system. The p roduction of bradykinin (BK) and the prostaglandins (PGs) may regulate init iation of pain. This study tested the hypothesis that BK and prostaglandin E-2 (PGE(2)) have a positive interaction in evoking neurosecretion of immun oreactive calcitonin gene-related peptide (iCGRP). Bovine dental pulp was p repared and stimulated by the superfusion method with BK alone and in combi nation with PGE(2). Kinin receptor antagonists to bradykinin-evoked release of iCGRP were also tested. Also tested was the hypothesis that dental pulp contains either the B-1 or B-2 or both BK receptors. Results showed that P GE, enhanced BK-evoked iCGRP release by more than 50%. Western immunoblots revealed detectable B-2 receptor protein with no detectable B-1 receptor pr otein. We conclude that BK evokes iCGRP release from bovine dental pulp whi ch is enhanced by a positive interaction with PGE(2). Neurosecretion is evo ked from isolated terminals of dental pulp fibers via the bradykinin B-2 re ceptor-dependent mechanism.