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Prostaglandin E2 Enhances Bradykinin-evoked iCGRP Release in Bovine Dental Pulp

Division of Endodontics, University of California-San Francisco, 707 Parnassus Avenue, San Francisco, CA 94143-0758, hgoodis{at}itsa.ucsf.edu

W.R. Bowles

Department of Endodontics, University of Minnesota, Minneapolis

K.M. Hargreaves

Department of Endodontics, University of Texas Health Science Center, San Antonio

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 cither the B, or B₂ or both BK receptors. Results showed that PGE₂ enhanced BK-evoked iCGRP release by more than 50%. Western immunoblots revealed detectable B, 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.

Key Words: prostaglandin E2 • bradykinin • pain • iCGRP • release.

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Journal of Dental Research, Vol. 79, No. 8, 1604-1607 (2000)
DOI: 10.1177/00220345000790081301


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