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. 2002 Jul;51(Suppl 1):i19–i23. doi: 10.1136/gut.51.suppl_1.i19

Visceral perception: inflammatory and non-inflammatory mediators

L Bueno, J Fioramonti
PMCID: PMC1867723  PMID: 12077058

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Figure 1 .

Figure 1

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Substances and major local pathways involved in triggering hyperalgesia to distension within the gut. Note that several mediators such as substance P (SP) may directly and indirectly influence the threshold of response of afferent fibres to a mechanical stimulus. CGRP, calcitonin gene related peptide; C5a, complement 5a; fMLP, formyl-methionyl-leucyl-phenylanine; IL, interleukin; NGF, nerve growth factor; NPY, neuropeptide Y; PGI2, prostacyclin I2; PGE 2, prostaglandin E2; TNF, tumour necrosis factor; VIP, vasoactive intestinal peptide; 5-HT, serotonin; 8(R),15(S)-diHETE, 8(R),15(S)-dihydroxyeicosatetraenoic acid. Modified from Coelho and colleagues.34

Figure 2 .

Figure 2

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Pathways, structures, and mediators involved in stress induced hyperalgesia to visceral (rectal) mechanical stimulus. ANS, autonomic nervous system; CRF, corticotrophin releasing factor; DRG, dorsal root ganglia; NKA, neurokinin A; SP, substance P; 5-HT, serotonin.

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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