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Received December 20, 2005
Revised January 9, 2006
Accepted after revision February 22, 2006
1 University of Oregon
* To whom correspondence should be addressed. E-mail: minson{at}oregon.uoregon.edu.
The initial skin blood flow response to rapid local heating is an axon reflex suggested to 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. Thirty nine 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 (1.0µM sodium nitroprusside, SNP), adrenergic blockade (10mM bretylium tosylate) and low dose (0.1µM) 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 sites, the axon reflex response was shifted to a higher temperature in four subjects in the L-NAME sites (37.0 ± 0.3°C, n=16 vs. 39.8 ± 0.1°C, n=4; P<0.001) and absent in twelve 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 (38.2 ± 0.5°C vs. 37.7 ± 0.4°C, P<0.05, n=5). These results suggest that endogenous NO and noradrenaline contribute to the temperature threshold of the axon reflex response during gradual local heating of the skin.
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