Systemic anti-inflammatory effect induced by counter-irritation through a local release of somatostatin from nociceptors

Research output: Contribution to journalArticle

78 Citations (Scopus)

Abstract

1. Neurogenic plasma extravasation evoked by topical application of 1% vv-1 mustard oil on the skin of the acutely denervated rat hindleg (primary reaction) inhibited the development of a subsequent oil-induced plasma extravasation induced in the skin of the contralateral hindleg by 49.3 ± 7.06% (n = 9) and in the conjunctival mucosa due to 0.1% wv-1 capsaicin instillation by 33.5 ± 10.05% (n = 6). The primary reaction also inhibited the non-neurogenic hindpaw oedema evoked by s.c. injection of 5% wv-1 dextran into the chronically denervated hindpaw by 48.0 ± 4.6% (n = 5). 2. Capsaicin injection (100 μg ml-1 in 50 μl. s.c.) into the acutely denervated hindleg caused 56.5 ± 4.0% (n = 5) inhibition in the intensity of plasma extravasation elicited by 1% vv-1 mustard oil smearing on the contralateral side. After chronic denervation, subplantar injection of 5% wv-1 dextran elicited a non-neurogenic inflammatory response with intensive tissue oedema without causing any systemic anti-inflammatory effect. Bilateral adrenalectomy did not inhibit the mustard oil-induced anti-inflammatory effect in the contralateral hindleg. 3. Pretreating the rats with polyclonal somatostatin antiserum (0.5 ml rat-1, i.v.) or with the somatostatin depleting agent cysteamine (250 mg kg-1, s.c.) prevented the inhibitory action of mustard oil-induced inflammation on subsequent neurogenic plasma extravasation and strongly diminished the inhibition of non-neurogenic oedema formation evoked by dextran. 4. Exogenous somatostatin (10 μg kg-1 i.p.) caused a 30.3 ± 8.3% (n = 6) inhibition of plasma extravasation caused by mustard oil smearing on the acutely denervated hindleg and this inhibitory effect was abolished by somatostatin antiserum (0.5 ml rat-1, i.v.). The plasma level of somatostatin-like immunoreactivity (SST-LI) increased by 40.03 ± 6.8% (n = 6) 10 min after topical application of 1% vv-1 mustard oil on the acutely denervated hindpaws compared to the paraffin oil treated control group. Chronic denervation of the hindlegs or cysteamine (280 mg kg-1, s.c.) pretreatment prevented the mustard oil-induced elevation of SST-LI in plasma. 5. It is concluded that chemical excitation of the capsaicin-sensitive sensory receptors not only induces local neurogenic plasma extravasation but also inhibits the development of a subsequent inflammatory reaction at remote sites of the body in the rat. A role for somatostatin in this systemic anti-inflammatory effect is suggested.

Original languageEnglish
Pages (from-to)916-922
Number of pages7
JournalBritish Journal of Pharmacology
Volume125
Issue number4
DOIs
Publication statusPublished - 1998

Fingerprint

Nociceptors
Somatostatin
Anti-Inflammatory Agents
Capsaicin
Cysteamine
Edema
Denervation
Injections
Immune Sera
Skin
Adrenalectomy
Sensory Receptor Cells
mustard oil
Dextrans
Oils
Mucous Membrane
Inflammation
Control Groups

Keywords

  • Anti-inflammatory effect
  • Capsaicin-sensitive primary afferent neurone
  • Cysteamine
  • Dextran-oedema
  • Mustard oil
  • Neurogenic inflammation
  • Somatostatin
  • Somatostatin antiserum

ASJC Scopus subject areas

  • Pharmacology

Cite this

@article{779540f31875461983b2e75eaa2900e1,
title = "Systemic anti-inflammatory effect induced by counter-irritation through a local release of somatostatin from nociceptors",
abstract = "1. Neurogenic plasma extravasation evoked by topical application of 1{\%} vv-1 mustard oil on the skin of the acutely denervated rat hindleg (primary reaction) inhibited the development of a subsequent oil-induced plasma extravasation induced in the skin of the contralateral hindleg by 49.3 ± 7.06{\%} (n = 9) and in the conjunctival mucosa due to 0.1{\%} wv-1 capsaicin instillation by 33.5 ± 10.05{\%} (n = 6). The primary reaction also inhibited the non-neurogenic hindpaw oedema evoked by s.c. injection of 5{\%} wv-1 dextran into the chronically denervated hindpaw by 48.0 ± 4.6{\%} (n = 5). 2. Capsaicin injection (100 μg ml-1 in 50 μl. s.c.) into the acutely denervated hindleg caused 56.5 ± 4.0{\%} (n = 5) inhibition in the intensity of plasma extravasation elicited by 1{\%} vv-1 mustard oil smearing on the contralateral side. After chronic denervation, subplantar injection of 5{\%} wv-1 dextran elicited a non-neurogenic inflammatory response with intensive tissue oedema without causing any systemic anti-inflammatory effect. Bilateral adrenalectomy did not inhibit the mustard oil-induced anti-inflammatory effect in the contralateral hindleg. 3. Pretreating the rats with polyclonal somatostatin antiserum (0.5 ml rat-1, i.v.) or with the somatostatin depleting agent cysteamine (250 mg kg-1, s.c.) prevented the inhibitory action of mustard oil-induced inflammation on subsequent neurogenic plasma extravasation and strongly diminished the inhibition of non-neurogenic oedema formation evoked by dextran. 4. Exogenous somatostatin (10 μg kg-1 i.p.) caused a 30.3 ± 8.3{\%} (n = 6) inhibition of plasma extravasation caused by mustard oil smearing on the acutely denervated hindleg and this inhibitory effect was abolished by somatostatin antiserum (0.5 ml rat-1, i.v.). The plasma level of somatostatin-like immunoreactivity (SST-LI) increased by 40.03 ± 6.8{\%} (n = 6) 10 min after topical application of 1{\%} vv-1 mustard oil on the acutely denervated hindpaws compared to the paraffin oil treated control group. Chronic denervation of the hindlegs or cysteamine (280 mg kg-1, s.c.) pretreatment prevented the mustard oil-induced elevation of SST-LI in plasma. 5. It is concluded that chemical excitation of the capsaicin-sensitive sensory receptors not only induces local neurogenic plasma extravasation but also inhibits the development of a subsequent inflammatory reaction at remote sites of the body in the rat. A role for somatostatin in this systemic anti-inflammatory effect is suggested.",
keywords = "Anti-inflammatory effect, Capsaicin-sensitive primary afferent neurone, Cysteamine, Dextran-oedema, Mustard oil, Neurogenic inflammation, Somatostatin, Somatostatin antiserum",
author = "J. Szolcs{\'a}nyi and E. Pint{\'e}r and Z. Helyes and G{\'a}bor Oroszi and J. N{\'e}meth",
year = "1998",
doi = "10.1038/sj.bjp.0702144",
language = "English",
volume = "125",
pages = "916--922",
journal = "British Journal of Pharmacology",
issn = "0007-1188",
publisher = "Wiley-Blackwell",
number = "4",

}

TY - JOUR

T1 - Systemic anti-inflammatory effect induced by counter-irritation through a local release of somatostatin from nociceptors

AU - Szolcsányi, J.

AU - Pintér, E.

AU - Helyes, Z.

AU - Oroszi, Gábor

AU - Németh, J.

PY - 1998

Y1 - 1998

N2 - 1. Neurogenic plasma extravasation evoked by topical application of 1% vv-1 mustard oil on the skin of the acutely denervated rat hindleg (primary reaction) inhibited the development of a subsequent oil-induced plasma extravasation induced in the skin of the contralateral hindleg by 49.3 ± 7.06% (n = 9) and in the conjunctival mucosa due to 0.1% wv-1 capsaicin instillation by 33.5 ± 10.05% (n = 6). The primary reaction also inhibited the non-neurogenic hindpaw oedema evoked by s.c. injection of 5% wv-1 dextran into the chronically denervated hindpaw by 48.0 ± 4.6% (n = 5). 2. Capsaicin injection (100 μg ml-1 in 50 μl. s.c.) into the acutely denervated hindleg caused 56.5 ± 4.0% (n = 5) inhibition in the intensity of plasma extravasation elicited by 1% vv-1 mustard oil smearing on the contralateral side. After chronic denervation, subplantar injection of 5% wv-1 dextran elicited a non-neurogenic inflammatory response with intensive tissue oedema without causing any systemic anti-inflammatory effect. Bilateral adrenalectomy did not inhibit the mustard oil-induced anti-inflammatory effect in the contralateral hindleg. 3. Pretreating the rats with polyclonal somatostatin antiserum (0.5 ml rat-1, i.v.) or with the somatostatin depleting agent cysteamine (250 mg kg-1, s.c.) prevented the inhibitory action of mustard oil-induced inflammation on subsequent neurogenic plasma extravasation and strongly diminished the inhibition of non-neurogenic oedema formation evoked by dextran. 4. Exogenous somatostatin (10 μg kg-1 i.p.) caused a 30.3 ± 8.3% (n = 6) inhibition of plasma extravasation caused by mustard oil smearing on the acutely denervated hindleg and this inhibitory effect was abolished by somatostatin antiserum (0.5 ml rat-1, i.v.). The plasma level of somatostatin-like immunoreactivity (SST-LI) increased by 40.03 ± 6.8% (n = 6) 10 min after topical application of 1% vv-1 mustard oil on the acutely denervated hindpaws compared to the paraffin oil treated control group. Chronic denervation of the hindlegs or cysteamine (280 mg kg-1, s.c.) pretreatment prevented the mustard oil-induced elevation of SST-LI in plasma. 5. It is concluded that chemical excitation of the capsaicin-sensitive sensory receptors not only induces local neurogenic plasma extravasation but also inhibits the development of a subsequent inflammatory reaction at remote sites of the body in the rat. A role for somatostatin in this systemic anti-inflammatory effect is suggested.

AB - 1. Neurogenic plasma extravasation evoked by topical application of 1% vv-1 mustard oil on the skin of the acutely denervated rat hindleg (primary reaction) inhibited the development of a subsequent oil-induced plasma extravasation induced in the skin of the contralateral hindleg by 49.3 ± 7.06% (n = 9) and in the conjunctival mucosa due to 0.1% wv-1 capsaicin instillation by 33.5 ± 10.05% (n = 6). The primary reaction also inhibited the non-neurogenic hindpaw oedema evoked by s.c. injection of 5% wv-1 dextran into the chronically denervated hindpaw by 48.0 ± 4.6% (n = 5). 2. Capsaicin injection (100 μg ml-1 in 50 μl. s.c.) into the acutely denervated hindleg caused 56.5 ± 4.0% (n = 5) inhibition in the intensity of plasma extravasation elicited by 1% vv-1 mustard oil smearing on the contralateral side. After chronic denervation, subplantar injection of 5% wv-1 dextran elicited a non-neurogenic inflammatory response with intensive tissue oedema without causing any systemic anti-inflammatory effect. Bilateral adrenalectomy did not inhibit the mustard oil-induced anti-inflammatory effect in the contralateral hindleg. 3. Pretreating the rats with polyclonal somatostatin antiserum (0.5 ml rat-1, i.v.) or with the somatostatin depleting agent cysteamine (250 mg kg-1, s.c.) prevented the inhibitory action of mustard oil-induced inflammation on subsequent neurogenic plasma extravasation and strongly diminished the inhibition of non-neurogenic oedema formation evoked by dextran. 4. Exogenous somatostatin (10 μg kg-1 i.p.) caused a 30.3 ± 8.3% (n = 6) inhibition of plasma extravasation caused by mustard oil smearing on the acutely denervated hindleg and this inhibitory effect was abolished by somatostatin antiserum (0.5 ml rat-1, i.v.). The plasma level of somatostatin-like immunoreactivity (SST-LI) increased by 40.03 ± 6.8% (n = 6) 10 min after topical application of 1% vv-1 mustard oil on the acutely denervated hindpaws compared to the paraffin oil treated control group. Chronic denervation of the hindlegs or cysteamine (280 mg kg-1, s.c.) pretreatment prevented the mustard oil-induced elevation of SST-LI in plasma. 5. It is concluded that chemical excitation of the capsaicin-sensitive sensory receptors not only induces local neurogenic plasma extravasation but also inhibits the development of a subsequent inflammatory reaction at remote sites of the body in the rat. A role for somatostatin in this systemic anti-inflammatory effect is suggested.

KW - Anti-inflammatory effect

KW - Capsaicin-sensitive primary afferent neurone

KW - Cysteamine

KW - Dextran-oedema

KW - Mustard oil

KW - Neurogenic inflammation

KW - Somatostatin

KW - Somatostatin antiserum

UR - http://www.scopus.com/inward/record.url?scp=0031728130&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031728130&partnerID=8YFLogxK

U2 - 10.1038/sj.bjp.0702144

DO - 10.1038/sj.bjp.0702144

M3 - Article

C2 - 9831933

AN - SCOPUS:0031728130

VL - 125

SP - 916

EP - 922

JO - British Journal of Pharmacology

JF - British Journal of Pharmacology

SN - 0007-1188

IS - 4

ER -