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Substance P May Pre-empt VIP in Regulating Temperature

located in specialized skin nerves. However, more work is necessary to clearly define its role in heat stress and other physiological responses.”

In the study, the participants were lying down and wearing water-perfused suits. Each person received various injections into the skin of one arm designed to desensitize the NK-1 receptor and block nitric oxide. This step was then followed by circulating heated water through the suit to raise core body temperatures to about 100 degrees Fahrenheit. The investigators then measured the changes in skin blood flow at the infusion sites.

Minson, co-director of the UO Exercise and Environmental Physiology Laboratories, and his doctoral student Brett J. Wong then analyzed the data. They found that desensitization of the NK-1 receptor pathway before body heating significantly reduced the rise in skin blood flow during subsequent heating. They also concluded that NK-1 receptor desensitization combined with the nitric-oxide inhibition caused additional reductions of blood flow. “This is an important distinction as it suggests more than one pathway is involved in the process,” Minson said.

In summary, Minson and Wong concluded that “NK-1 receptors contribute to active vasodilation [the rise in skin blood flow] and that a combined NK-1 receptor desensitization and nitric oxide inhibition further diminishes active vasodilation.” However, Minson cautioned: “It’s very likely that there is more than one neurotransmitter involved because of the redundancy of the system. We still don’t know the specifics of how the rise in blood flow is tied to sweating.”

The research, conducted primarily by Wong, was a direct follow-up to a study that appeared in the November 2004 issue of the Journal of Physiology. In that paper, Wong, Minson and additional colleagues reported that the histamine 1 receptor, which is involved in seasonal allergies, has a role in skin blood flow changes during heat stress.

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