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Journal of Neuroscience, Vol 14, 4329-4337, Copyright © 1994 by Society for Neuroscience
Sodium nitroprusside evokes the release of immunoreactive calcitonin gene-related peptide and substance P from dorsal horn slices via nitric oxide-dependent and nitric oxide-independent mechanisms
MG Garry, JD Richardson and KM Hargreaves
Department of Restorative Sciences, University of Minnesota Dental School, Minneapolis 55455.
The results of behavioral studies suggest that nitric oxide (NO)
participates in certain spinal mechanisms that contribute to hyperalgesia.
Additionally, previous studies indicate that the release of immunoreactive
calcitonin gene-related peptide (iCGRP) and substance P (iSP) is increased
in the dorsal horn of the spinal cord during hyperalgesia. Therefore, the
aim of this study was to determine whether NO acts to enhance peptide
release in the dorsal horn of rats using an in vitro superfusion technique.
Sodium nitroprusside (SNP) was used as an NO donor. The results of this
study indicate that SNP caused a dose- related, calcium-dependent increase
in the release of iCGRP and iSP from dorsal horn slices of the rat spinal
cord. Furthermore, pretreatment with SNP reduced the ability of capsaicin
to evoke the release of either peptide, suggesting that a target for SNP
exists on certain capsaicin-sensitive primary afferent terminals. In
addition to increasing peptide release, SNP also caused a significant five
to sixfold increase in the levels of immunoreactive guanosine 3',5'-
monophosphate (i-cGMP) in the dorsal horn. This SNP-evoked increase was
significantly decreased by the guanylate cyclase inhibitor methylene blue
in a dose-dependent manner. In addition, the release of iCGRP was also
significantly reduced in the presence of methylene blue, although the
relationship between peptide release and i-cGMP production remains unclear.
Sodium nitroprusside-evoked peptide release was significantly reduced in
the presence of hemoglobin (an oxide radical scavenger), suggesting that
the drug effect was due to the generation of NO. However, the release of
iCGRP and iSP was also evoked by sodium ferricyanide (the coproduct of SNP)
and by 7-d-old, photoinactivated SNP.(ABSTRACT TRUNCATED AT 250 WORDS)
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