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Journal of Neuroscience, Vol 14, 4987-4997, Copyright © 1994 by Society for Neuroscience
Prostaglandin E2 enhances bradykinin-stimulated release of neuropeptides from rat sensory neurons in culture
MR Vasko, WB Campbell and KJ Waite
Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis 46202-5120.
Prostaglandins are known to enhance the inflammatory and nociceptive
actions of other chemical mediators of inflammation such as bradykinin. One
possible mechanism for this sensitizing action is that prostanoids augment
the release of neuroactive substances from sensory neurons. To initially
test this hypothesis, we examined whether selected prostaglandins could
enhance the resting or bradykinin-evoked release of immunoreactive
substance P (iSP) and/or immunoreactive calcitonin gene-related peptide
(iCGRP) from sensory neurons in culture. Bradykinin alone causes a
concentration-dependent increase in the release of iSP and iCGRP from
isolated sensory neurons, and this action is abolished in the absence of
extracellular calcium. Pretreating the neurons with PGE2 (10 nM to 1
microM) potentiates the bradykinin-evoked release of both iSP and iCGRP by
approximately two-to fourfold. At these concentrations, PGE2 alone did not
significantly alter peptide release. Exposing the cultures to 1 microM PGF2
alpha is ineffective in altering either resting or bradykinin-evoked
peptide release. Sensory neurons in culture contain cyclooxygenase-like
immunoreactivity suggesting that the enzyme that converts arachidonic acid
to prostaglandins is present. In addition, pretreating cultures with 14C-
arachidonic acid yields radiolabeled eicosanoids that cochromatograph with
known prostaglandin standards. Preexposing cultures to indomethacin
abolishes the production of prostaglandins and attenuates the
bradykinin-stimulated release of iSP and iCGRP. This implies that the
synthesis of prostaglandins contributes to the bradykinin-evoked release of
peptides. The augmentation of bradykinin-induced release of iSP and iCGRP
by PGE2 may be one mechanism to account for the inflammatory and
hyperalgesic actions of this eicosanoid.
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