Peripheral Contributions to Visceral Hyperalgesia
Hyperalgesia has long been recognized clinically as a consequence of tissue injury. Primary hyperalgesia (arising from the site of injury) is generally considered to be due to sensitization of sensory receptors (eg, nociceptors) and perhaps activation of so-called ‘silent nociceptors’ by mediators r...
Saved in:
| Main Author: | |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wiley
1999-01-01
|
| Series: | Canadian Journal of Gastroenterology |
| Online Access: | http://dx.doi.org/10.1155/1999/730765 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1832558425625591808 |
|---|---|
| author | GF Gebhart |
| author_facet | GF Gebhart |
| author_sort | GF Gebhart |
| collection | DOAJ |
| description | Hyperalgesia
has long been recognized clinically as a consequence of tissue
injury. Primary hyperalgesia (arising from the site of injury) is
generally considered to be due to sensitization of sensory receptors
(eg, nociceptors) and perhaps activation of so-called ‘silent
nociceptors’ by mediators released, synthesized or attracted to the
site of tissue injury. Key questions associated with understanding
visceral hyperalgesia relate to whether the viscera are innervated
by nociceptors (ie, sensory receptors that respond selectively to
noxious intensities of stimulation), whether visceral receptors
and/or afferent fibres sensitize after tissue injury and whether silent
nociceptors exist in the viscera. Studies in nonhuman animals
have revealed that hollow organs such as the esophagus,
gall bladder, stomach, urinary bladder, colon and uterus are
innervated by mechanically sensitive receptors with low or high
thresholds for response. Accordingly, it appears that the viscera
are innervated by nociceptors, although the issue is far from settled.
One characteristic of cutaneous nociceptors is their ability to
be sensitized when tissue is injured. Mechanosensitive visceral receptors
also sensitize when the viscera are experimentally inflamed,
but both visceral receptors with low thresholds and those
with high thresholds for response are sensitized. Moreover, it is often
not appreciated that visceral receptors are likely polymodal
rather than unimodal – that is, mechanically sensitive visceral receptors
typically are also sensitive to chemical and/or thermal
stimuli. In this sense, visceral receptors may be considered
evolutionarily older than more highly developed, specialized cutaneous
receptors. Finally, there are mechanically insensitive receptors
that innervate the viscera and, when tissue is injured, develop
spontaneous activity and acquire sensitivity to mechanical stimuli.
In the aggregrate, visceral receptors change their behaviour in
the presence of tissue injury and, along with activated mechanically
insensitive receptors, increase the afferent barrage into the
spinal cord, contributing to the development of visceral
hyperalgesia. |
| format | Article |
| id | doaj-art-fcdf07a15fe243579d6b8d2fb1827187 |
| institution | Kabale University |
| issn | 0835-7900 |
| language | English |
| publishDate | 1999-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Canadian Journal of Gastroenterology |
| spelling | doaj-art-fcdf07a15fe243579d6b8d2fb18271872025-02-03T01:32:30ZengWileyCanadian Journal of Gastroenterology0835-79001999-01-0113Suppl A37A41A10.1155/1999/730765Peripheral Contributions to Visceral HyperalgesiaGF Gebhart0Department of Pharmacology, College of Medicine, University of Iowa, Iowa City, Iowa 52242-1109, USAHyperalgesia has long been recognized clinically as a consequence of tissue injury. Primary hyperalgesia (arising from the site of injury) is generally considered to be due to sensitization of sensory receptors (eg, nociceptors) and perhaps activation of so-called ‘silent nociceptors’ by mediators released, synthesized or attracted to the site of tissue injury. Key questions associated with understanding visceral hyperalgesia relate to whether the viscera are innervated by nociceptors (ie, sensory receptors that respond selectively to noxious intensities of stimulation), whether visceral receptors and/or afferent fibres sensitize after tissue injury and whether silent nociceptors exist in the viscera. Studies in nonhuman animals have revealed that hollow organs such as the esophagus, gall bladder, stomach, urinary bladder, colon and uterus are innervated by mechanically sensitive receptors with low or high thresholds for response. Accordingly, it appears that the viscera are innervated by nociceptors, although the issue is far from settled. One characteristic of cutaneous nociceptors is their ability to be sensitized when tissue is injured. Mechanosensitive visceral receptors also sensitize when the viscera are experimentally inflamed, but both visceral receptors with low thresholds and those with high thresholds for response are sensitized. Moreover, it is often not appreciated that visceral receptors are likely polymodal rather than unimodal – that is, mechanically sensitive visceral receptors typically are also sensitive to chemical and/or thermal stimuli. In this sense, visceral receptors may be considered evolutionarily older than more highly developed, specialized cutaneous receptors. Finally, there are mechanically insensitive receptors that innervate the viscera and, when tissue is injured, develop spontaneous activity and acquire sensitivity to mechanical stimuli. In the aggregrate, visceral receptors change their behaviour in the presence of tissue injury and, along with activated mechanically insensitive receptors, increase the afferent barrage into the spinal cord, contributing to the development of visceral hyperalgesia.http://dx.doi.org/10.1155/1999/730765 |
| spellingShingle | GF Gebhart Peripheral Contributions to Visceral Hyperalgesia Canadian Journal of Gastroenterology |
| title | Peripheral Contributions to Visceral Hyperalgesia |
| title_full | Peripheral Contributions to Visceral Hyperalgesia |
| title_fullStr | Peripheral Contributions to Visceral Hyperalgesia |
| title_full_unstemmed | Peripheral Contributions to Visceral Hyperalgesia |
| title_short | Peripheral Contributions to Visceral Hyperalgesia |
| title_sort | peripheral contributions to visceral hyperalgesia |
| url | http://dx.doi.org/10.1155/1999/730765 |
| work_keys_str_mv | AT gfgebhart peripheralcontributionstovisceralhyperalgesia |