Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2008632 | Peptides | 2006 | 8 Pages |
Abstract
The N-terminal metabolite of the undecapeptide substance P (SP), substance P1-7 (SP1-7), is known to modulate nociception in the central nervous system (CNS) and often has opposite effects from SP. This study investigated the ability of SP1-7 to modulate the vasodilatation response to SP in anaesthetized rats under different injury conditions using a blister model of inflammation on the hind footpad. The results indicated that SP1-7 inhibited the vascular response to SP in a dose-dependent manner. The putative antagonists naloxone and d-Pro2-d-Phe7-SP1-7 (d-SP1-7) reversed the effect of SP1-7. d-SP1-7 improved the responsiveness to SP under chronic nerve injury, which suggests a role for endogenous SP1-7 in this model. SP1-7 did not inhibit the response to electrical stimulation of the sciatic nerve, which indicates that the heptapeptide interacts at a post-terminal binding site. The current results suggest that SP1-7 may have inhibitory properties in inflammation, analogous to its antinociceptive role in the central nervous system.
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Authors
Daniel Wiktelius, Zeinab Khalil, Fred Nyberg,