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Seegers HC, Hood VC, Kidd BL, et al. Enhancement of angiogenesis by endogenous substance P release and neurokinin-1 receptors during neurogenic inflammation. J Pharmacol Exp Ther. 2003;306(1):8-12doi: 10.1124/jpet.103.050013.
Seegers, H. C., Hood, V. C., Kidd, B. L., Cruwys, S. C., & Walsh, D. A. (2003). Enhancement of angiogenesis by endogenous substance P release and neurokinin-1 receptors during neurogenic inflammation. The Journal of pharmacology and experimental therapeutics, 306(1), 8-12. https://doi.org/10.1124/jpet.103.050013
Seegers, Hélène C, et al. "Enhancement of angiogenesis by endogenous substance P release and neurokinin-1 receptors during neurogenic inflammation." The Journal of pharmacology and experimental therapeutics vol. 306,1 (2003): 8-12. doi: https://doi.org/10.1124/jpet.103.050013
Seegers HC, Hood VC, Kidd BL, Cruwys SC, Walsh DA. Enhancement of angiogenesis by endogenous substance P release and neurokinin-1 receptors during neurogenic inflammation. J Pharmacol Exp Ther. 2003 Jul;306(1):8-12. doi: 10.1124/jpet.103.050013. Epub 2003 Mar 26. PMID: 12660314.
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J Pharmacol Exp Ther. 2003 Jul;306(1):8-12. doi: 10.1124/jpet.103.050013. Epub 2003 Mar 26.

Enhancement of angiogenesis by endogenous substance P release and neurokinin-1 receptors during neurogenic inflammation.

The Journal of pharmacology and experimental therapeutics

Hélène C Seegers, Vivienne C Hood, Bruce L Kidd, Simon C Cruwys, David A Walsh

Affiliations

  1. Academic Rheumatology, University of Nottingham Clinical Sciences Building, City Hospital, Hucknall Road, Nottingham, NG5 1PB, UK.

PMID: 12660314 DOI: 10.1124/jpet.103.050013

Abstract

Early angiogenesis is a key step in the transition from acute to persistent inflammation. The nervous system has long been known to play a role in inflammation, in part through the release of substance P from peripheral nerve terminals (neurogenic inflammation). Application of substance P can stimulate vessel growth in a variety of angiogenesis assays, although it was previously not known whether endogenous substance P released from sensory nerves could modulate angiogenesis. We hypothesized that endogenous substance P can initiate angiogenesis during acute neurogenic inflammation. Here we show that 10 nmol of substance P can stimulate angiogenesis within the rat knee synovium, as shown by increased endothelial cell proliferation index [PCNA index, 19% (95% confidence interval (CI), 17 to 20%)] compared with saline injected knees [6% (95% CI, 4% to 8%), p < 0.05]. Moreover, this was prevented by coadministration of an antagonist of the neurokinin-1 (NK1) subtype of neurokinin receptor SR140333 (nolpitantium), 1 micro mol [8% (95% CI, 5% to 11%)]. Capsaicin 0.5%, which stimulates release of endogenous substance P from sensory nerves, was also found to enhance synovial angiogenesis, [PCNA index 17% (95% CI, 14% to 19%)] compared with saline injected control knees [2% (95% CI, 1% to 3%), p < 0.05], and this also was inhibited by 1 micro mol of SR140333 [11% (95% CI, 8 to 16%)]. Inhibition of capsaicin-enhanced angiogenesis was incomplete, and this may indicate a contribution of other neuropeptides, in addition to substance P-NK1 receptor interactions, in capsaicin-enhanced angiogenesis. NK1 receptor antagonists could have therapeutic potential in conditions where neurogenic angiogenesis contributes to disease.

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