Prostaglandin E2 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 production of bradykinin (BK) and the prostaglandins (PGs) may regulate initiation of pain. This study tested the hypothesis that BK and prostaglandin E2 (PGE2) have a positive interaction in evoking neurosecretion of immunoreactive calcitonin gene-related peptide (iCGRP). Bovine dental pulp was prepared and stimulated by the superfusion method with BK alone and in combination with PGE2. Kinin receptor antagonists to bradykinin-evoked release of iCGRP were also tested. Also tested was the hypothesis that dental pulp contains either the B1 or B2 or both BK receptors. Results showed that PGE2 enhanced BK-evoked iCGRP release by more than 50%. Western immunoblots revealed detectable B2 receptor protein with no detectable B1 receptor protein. We conclude that BK evokes iCGRP release from bovine dental pulp which is enhanced by a positive interaction with PGE2. Neurosecretion is evoked from isolated terminals of dental pulp fibers via the bradykinin B2 receptor-dependent mechanism.[1]References
- Prostaglandin E2 enhances bradykinin-evoked iCGRP release in bovine dental pulp. Goodis, H.E., Bowles, W.R., Hargreaves, K.M. J. Dent. Res. (2000) [Pubmed]
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