Abstract

The mechanisms underlying the reduction in cutaneous blood flow in response to cooling are only partially understood. A study published in this issue of the British Journal of Pharmacology now provides evidence for the involvement of excitatory P2-receptors located at sympathetic axon terminals in the cooling-induced vasoconstriction in the skin. Cooling appears to cause the release of adenine nucleotides followed by the activation of excitatory presynaptic P2-receptors at noradrenergic axon terminals. Activation of these excitatory P2-receptors induces the release of noradrenaline, which subsequently causes constriction of blood vessels in the skin by action on smooth muscle alpha(1)- and alpha(2)-adrenoceptors. The commentary discusses the implication of the results and remaining questions.

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