Effects of capsaicin, bradykinin and prostaglandin E2 in the human skin
Wallengren, Joanna LU
and Håkanson, Rolf
LU
(1992)
In British Journal of Dermatology
126(2).
p.111-117
- Abstract
- The actions and interactions of putative mediators of inflammation, such as substance P (SP), histamine, bradykinin and prostaglandins (PGE2) were studied in human skin. In addition, the effects of capsaicin were examined as it is known to release (and to deplete) SP and calcitonin gene-related peptide from C-fibres. The flare evoked by bradykinin was abolished by pretreatment with lignocaine (local anesthetic), compound 48/80 (mast-cell histamine liberator), mepyramine (H1-receptor antagonist) and indomethacin (cyclo-oxygenase inhibitor) but was unaffected by atropine and ketanserin (serotonin antagonist). The weal response was not reduced by any of the drugs. The flare evoked by capsaicin was abolished by lignocaine and indomethacin but... (More)
- The actions and interactions of putative mediators of inflammation, such as substance P (SP), histamine, bradykinin and prostaglandins (PGE2) were studied in human skin. In addition, the effects of capsaicin were examined as it is known to release (and to deplete) SP and calcitonin gene-related peptide from C-fibres. The flare evoked by bradykinin was abolished by pretreatment with lignocaine (local anesthetic), compound 48/80 (mast-cell histamine liberator), mepyramine (H1-receptor antagonist) and indomethacin (cyclo-oxygenase inhibitor) but was unaffected by atropine and ketanserin (serotonin antagonist). The weal response was not reduced by any of the drugs. The flare evoked by capsaicin was abolished by lignocaine and indomethacin but was unaffected by compound 48/80, mepyramine, atropine and ketanserin. The weal response was reduced by indomethacin. The flare response to bradykinin seems to reflect the activation of C-fibres and associated mast cells, while the flare response to capsaicin seems to reflect the activation of C-fibres only. Repeated injections of capsaicin and bradykinin produced tachyphylaxis (and cross-tachyphylaxis) and greatly reduced the SP-evoked flare. Capsaicin produced tachyphylaxis also after treatment of the skin with a local anaesthetic, suggesting that it develops independently of C-fibre impulse flow. The tachyphylaxis produced by bradykinin and capsaicin seems to reflect the depletion of messenger peptides from the C-fibres. The flare response to SP following capsaicin- or bradykinin-induced desensitization gradually returned to normal after 5-8 weeks. The erythema evoked by PGE2 was reduced by 30% following pretreatment with lignocaine, mepyramine or compound 48/80. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/2088b5e4-79b1-47e8-9376-e69cd5770e57
- author
- Wallengren, Joanna
LU
and Håkanson, Rolf
LU
- organization
- publishing date
- 1992
- type
- Contribution to journal
- publication status
- published
- subject
- in
- British Journal of Dermatology
- volume
- 126
- issue
- 2
- pages
- 111 - 117
- publisher
- Wiley-Blackwell
- external identifiers
-
- scopus:0026547079
- ISSN
- 1365-2133
- DOI
- 10.1111/j.1365-2133.1992.tb07806.x
- language
- English
- LU publication?
- yes
- id
- 2088b5e4-79b1-47e8-9376-e69cd5770e57
- date added to LUP
- 2019-07-17 16:10:20
- date last changed
- 2021-09-26 04:03:08
@article{2088b5e4-79b1-47e8-9376-e69cd5770e57,
abstract = {{The actions and interactions of putative mediators of inflammation, such as substance P (SP), histamine, bradykinin and prostaglandins (PGE2) were studied in human skin. In addition, the effects of capsaicin were examined as it is known to release (and to deplete) SP and calcitonin gene-related peptide from C-fibres. The flare evoked by bradykinin was abolished by pretreatment with lignocaine (local anesthetic), compound 48/80 (mast-cell histamine liberator), mepyramine (H1-receptor antagonist) and indomethacin (cyclo-oxygenase inhibitor) but was unaffected by atropine and ketanserin (serotonin antagonist). The weal response was not reduced by any of the drugs. The flare evoked by capsaicin was abolished by lignocaine and indomethacin but was unaffected by compound 48/80, mepyramine, atropine and ketanserin. The weal response was reduced by indomethacin. The flare response to bradykinin seems to reflect the activation of C-fibres and associated mast cells, while the flare response to capsaicin seems to reflect the activation of C-fibres only. Repeated injections of capsaicin and bradykinin produced tachyphylaxis (and cross-tachyphylaxis) and greatly reduced the SP-evoked flare. Capsaicin produced tachyphylaxis also after treatment of the skin with a local anaesthetic, suggesting that it develops independently of C-fibre impulse flow. The tachyphylaxis produced by bradykinin and capsaicin seems to reflect the depletion of messenger peptides from the C-fibres. The flare response to SP following capsaicin- or bradykinin-induced desensitization gradually returned to normal after 5-8 weeks. The erythema evoked by PGE2 was reduced by 30% following pretreatment with lignocaine, mepyramine or compound 48/80.}},
author = {{Wallengren, Joanna and Håkanson, Rolf}},
issn = {{1365-2133}},
language = {{eng}},
number = {{2}},
pages = {{111--117}},
publisher = {{Wiley-Blackwell}},
series = {{British Journal of Dermatology}},
title = {{Effects of capsaicin, bradykinin and prostaglandin E2 in the human skin}},
url = {{http://dx.doi.org/10.1111/j.1365-2133.1992.tb07806.x}},
doi = {{10.1111/j.1365-2133.1992.tb07806.x}},
volume = {{126}},
year = {{1992}},
}