von Kügelgen Ivar
Department of Pharmacology, University of Bonn, Reuterstrasse 2b, Bonn D-53113, Germany.
Br J Pharmacol. 2006 Jul;148(5):561-2. doi: 10.1038/sj.bjp.0706767. Epub 2006 May 15.
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.
皮肤血流对冷却作出反应时减少的潜在机制仅得到部分理解。本期《英国药理学杂志》发表的一项研究现在提供了证据,表明位于交感神经轴突末端的兴奋性P2受体参与了皮肤冷却诱导的血管收缩。冷却似乎导致腺嘌呤核苷酸的释放,随后去甲肾上腺素能轴突末端的兴奋性突触前P2受体被激活。这些兴奋性P2受体的激活诱导去甲肾上腺素的释放,去甲肾上腺素随后通过作用于平滑肌α(1)和α(2)肾上腺素能受体而导致皮肤血管收缩。该评论讨论了这些结果的意义以及尚存的问题。