A cold 'sensor' which triggers the skin's vascular response to the cold could represent a new therapeutic target for the treatment of frostbite and hypothermia, according to scientists at King's College London. The study explains TRPA1's role in cold exposure and provides impetus for further research into how this gene could be targeted to enhance the body's protective response to cold.
The human body has several defense mechanisms to try and boost its core temperature in cold weather. The skin responds by narrowing its blood vessels to constrict the supply of blood (vasoconstriction) and retain body heat. Then vasodilatation i.e. blood vessels are widened and more blood flows to the surface of the skin. This process is important for keeping the skin warm. In extreme cold blood flow to the skin is disrupted leading to frostbite or swelling (chilblains).
In the King's study, the skin of anaesthetized mice was exposed to cold by immersing a paw in water. Blood flow was measured before and after exposure to the cold. Researchers found that TRPA1 gene acted in two distinct ways - first by sensing the change in temperature, and then by stimulating the protective constriction of blood vessels. The subsequent vasodilatation phase was also dependent on TRPA1 gene activation and was crucial for restoring blood flow to the skin.
Professor Peter Weissberg, Medical Director at the British Heart Foundation, which part-funded the research, said, "This study helps us to understand how and why our blood vessels contract and expand, and could help scientists develop treatments for many conditions where blood vessel or 'vascular' health is important, from Raynaud's to heart failure."
The study is published in 'Nature Communications'.