Nitric oxide and noradrenaline contribute to the temperature threshold of the axon reflex response to gradual local heating in human skin

Belinda McCully, Jessica R. Meendering, Brett J. Wong, Christopher T. Minson

Research output: Contribution to journalArticle

90 Citations (Scopus)

Abstract

The initial skin blood flow response to rapid local heating is an axon reflex, which may be mediated by calcitonin gene-related peptide and substance P released from C-fibres. We investigated the role of nitric oxide (NO) and noradrenaline on the temperature threshold for the axon reflex during gradual local heating. 36 subjects participated in two studies. Using microdialysis, we examined the following interventions: NO synthase inhibition (10mM NG-nitro-L-arginine methyl ester, L-NAME); low-dose NO infusion (1.0 μM sodium nitroprusside, SNP); adrenergic blockade (10mM bretylium tosylate); and low-dose (0.1 μM) noradrenaline infusion. Laser-Doppler flowmetry was used to measure red blood cell flux. Skin was heated at a rate of 0.1°C min-1 from 33°C to 40°C. Compared to control skin sites, the axon reflex response was shifted to a higher temperature in 4 subjects in the L-NAME sites (control, 37.0 ± 0.3.C, n=16; L-NAME, 39.8 ± 0.1.C, n=4; P < 0.001) and absent in 12 subjects. The response was also absent in L-NAME plus low-dose SNP sites and not altered by low-dose SNP infusion alone. Adrenergic blockade, with and without low-dose noradrenaline infusion, also abolished the axon reflex response in all subjects. Low-dose noradrenaline infusion alone shifted the axon reflex to a significantly lower temperature threshold compared to control sites (control, 38.2 ± 0.5.C; noradrenaline, 37.7 ± 0.4.C, P < 0.05, n=5). These results suggest that endogenous NO and noradrenaline contribute tothe temperature threshold of the axon reflex response during gradual local heating of the skin.

Original languageEnglish (US)
Pages (from-to)811-820
Number of pages10
JournalJournal of Physiology
Volume572
Issue number3
DOIs
StatePublished - May 1 2006
Externally publishedYes

Fingerprint

Heating
NG-Nitroarginine Methyl Ester
Axons
Reflex
Norepinephrine
Nitric Oxide
Skin
Temperature
Nitroprusside
Adrenergic Agents
Bretylium Tosylate
Unmyelinated Nerve Fibers
Laser-Doppler Flowmetry
Calcitonin Gene-Related Peptide
Microdialysis
Substance P
Nitric Oxide Synthase
Erythrocytes

ASJC Scopus subject areas

  • Physiology

Cite this

Nitric oxide and noradrenaline contribute to the temperature threshold of the axon reflex response to gradual local heating in human skin. / McCully, Belinda; Meendering, Jessica R.; Wong, Brett J.; Minson, Christopher T.

In: Journal of Physiology, Vol. 572, No. 3, 01.05.2006, p. 811-820.

Research output: Contribution to journalArticle

@article{af2d205e4f6c45ca8a20bbf477b83698,
title = "Nitric oxide and noradrenaline contribute to the temperature threshold of the axon reflex response to gradual local heating in human skin",
abstract = "The initial skin blood flow response to rapid local heating is an axon reflex, which may be mediated by calcitonin gene-related peptide and substance P released from C-fibres. We investigated the role of nitric oxide (NO) and noradrenaline on the temperature threshold for the axon reflex during gradual local heating. 36 subjects participated in two studies. Using microdialysis, we examined the following interventions: NO synthase inhibition (10mM NG-nitro-L-arginine methyl ester, L-NAME); low-dose NO infusion (1.0 μM sodium nitroprusside, SNP); adrenergic blockade (10mM bretylium tosylate); and low-dose (0.1 μM) noradrenaline infusion. Laser-Doppler flowmetry was used to measure red blood cell flux. Skin was heated at a rate of 0.1°C min-1 from 33°C to 40°C. Compared to control skin sites, the axon reflex response was shifted to a higher temperature in 4 subjects in the L-NAME sites (control, 37.0 ± 0.3.C, n=16; L-NAME, 39.8 ± 0.1.C, n=4; P < 0.001) and absent in 12 subjects. The response was also absent in L-NAME plus low-dose SNP sites and not altered by low-dose SNP infusion alone. Adrenergic blockade, with and without low-dose noradrenaline infusion, also abolished the axon reflex response in all subjects. Low-dose noradrenaline infusion alone shifted the axon reflex to a significantly lower temperature threshold compared to control sites (control, 38.2 ± 0.5.C; noradrenaline, 37.7 ± 0.4.C, P < 0.05, n=5). These results suggest that endogenous NO and noradrenaline contribute tothe temperature threshold of the axon reflex response during gradual local heating of the skin.",
author = "Belinda McCully and Meendering, {Jessica R.} and Wong, {Brett J.} and Minson, {Christopher T.}",
year = "2006",
month = "5",
day = "1",
doi = "10.1113/jphysiol.2005.104067",
language = "English (US)",
volume = "572",
pages = "811--820",
journal = "Journal of Physiology",
issn = "0022-3751",
publisher = "Wiley-Blackwell",
number = "3",

}

TY - JOUR

T1 - Nitric oxide and noradrenaline contribute to the temperature threshold of the axon reflex response to gradual local heating in human skin

AU - McCully, Belinda

AU - Meendering, Jessica R.

AU - Wong, Brett J.

AU - Minson, Christopher T.

PY - 2006/5/1

Y1 - 2006/5/1

N2 - The initial skin blood flow response to rapid local heating is an axon reflex, which may be mediated by calcitonin gene-related peptide and substance P released from C-fibres. We investigated the role of nitric oxide (NO) and noradrenaline on the temperature threshold for the axon reflex during gradual local heating. 36 subjects participated in two studies. Using microdialysis, we examined the following interventions: NO synthase inhibition (10mM NG-nitro-L-arginine methyl ester, L-NAME); low-dose NO infusion (1.0 μM sodium nitroprusside, SNP); adrenergic blockade (10mM bretylium tosylate); and low-dose (0.1 μM) noradrenaline infusion. Laser-Doppler flowmetry was used to measure red blood cell flux. Skin was heated at a rate of 0.1°C min-1 from 33°C to 40°C. Compared to control skin sites, the axon reflex response was shifted to a higher temperature in 4 subjects in the L-NAME sites (control, 37.0 ± 0.3.C, n=16; L-NAME, 39.8 ± 0.1.C, n=4; P < 0.001) and absent in 12 subjects. The response was also absent in L-NAME plus low-dose SNP sites and not altered by low-dose SNP infusion alone. Adrenergic blockade, with and without low-dose noradrenaline infusion, also abolished the axon reflex response in all subjects. Low-dose noradrenaline infusion alone shifted the axon reflex to a significantly lower temperature threshold compared to control sites (control, 38.2 ± 0.5.C; noradrenaline, 37.7 ± 0.4.C, P < 0.05, n=5). These results suggest that endogenous NO and noradrenaline contribute tothe temperature threshold of the axon reflex response during gradual local heating of the skin.

AB - The initial skin blood flow response to rapid local heating is an axon reflex, which may be mediated by calcitonin gene-related peptide and substance P released from C-fibres. We investigated the role of nitric oxide (NO) and noradrenaline on the temperature threshold for the axon reflex during gradual local heating. 36 subjects participated in two studies. Using microdialysis, we examined the following interventions: NO synthase inhibition (10mM NG-nitro-L-arginine methyl ester, L-NAME); low-dose NO infusion (1.0 μM sodium nitroprusside, SNP); adrenergic blockade (10mM bretylium tosylate); and low-dose (0.1 μM) noradrenaline infusion. Laser-Doppler flowmetry was used to measure red blood cell flux. Skin was heated at a rate of 0.1°C min-1 from 33°C to 40°C. Compared to control skin sites, the axon reflex response was shifted to a higher temperature in 4 subjects in the L-NAME sites (control, 37.0 ± 0.3.C, n=16; L-NAME, 39.8 ± 0.1.C, n=4; P < 0.001) and absent in 12 subjects. The response was also absent in L-NAME plus low-dose SNP sites and not altered by low-dose SNP infusion alone. Adrenergic blockade, with and without low-dose noradrenaline infusion, also abolished the axon reflex response in all subjects. Low-dose noradrenaline infusion alone shifted the axon reflex to a significantly lower temperature threshold compared to control sites (control, 38.2 ± 0.5.C; noradrenaline, 37.7 ± 0.4.C, P < 0.05, n=5). These results suggest that endogenous NO and noradrenaline contribute tothe temperature threshold of the axon reflex response during gradual local heating of the skin.

UR - http://www.scopus.com/inward/record.url?scp=33645822812&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33645822812&partnerID=8YFLogxK

U2 - 10.1113/jphysiol.2005.104067

DO - 10.1113/jphysiol.2005.104067

M3 - Article

C2 - 16497714

AN - SCOPUS:33645822812

VL - 572

SP - 811

EP - 820

JO - Journal of Physiology

JF - Journal of Physiology

SN - 0022-3751

IS - 3

ER -