Excitatory P2-receptors at sympathetic axon terminals: role in temperature control of cutaneous blood flow.
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.
von Kügelgen
Ivar
I
Department of Pharmacology, University of Bonn, Reuterstrasse 2b, Bonn D-53113, Germany. kugelgen@uni-bonn.de
D000320:Adrenergic Fibers / Q000502:physiology*; D001831:Body Temperature / Q000502:physiology; D001833:Body Temperature Regulation / Q000502:physiology*; D020405:Dermis / Q000098:blood supply*; D006801:Humans; D017729:Presynaptic Terminals / Q000502:physiology*; D018048:Receptors, Purinergic P2 / Q000502:physiology*; D012039:Regional Blood Flow / Q000502:physiology; D012881:Skin Temperature; D014661:Vasoconstriction / Q000502:physiology
D018048:Receptors, Purinergic P2