Nociceptors in cardiovascular functions: complex interplay as a result of cyclooxygenase inhibition.
Nociceptors in cardiovascular functions: complex interplay as a result of cyclooxygenase inhibition.
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DOI：
10.1186/1744-8069-2-26
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发表时间：
2006-08-17
期刊：
影响因子：
3.3
通讯作者：
Raisinghani M
中科院分区：
文献类型：
--
作者：
Premkumar LS;Raisinghani M
前列腺素（PG）是炎性疼痛的必要成分，如环氧合酶1/2（COX 1/2）抑制剂的疗效所示。PG不直接激活伤害性离子通道，而是通过与G蛋白偶联受体相关的下游机制使其敏感。抗炎作用据称是由抑制促炎剂的合成和/或释放引起的。这些药剂从感觉神经元的外周和中央末端的释放分别调节来自外周的伤害性输入和第一感觉突触处的突触传递。心脏和血管由表达化学、机械和温度敏感受体的感觉神经末梢密集支配。这些受体的激活通过其Ca 2+渗透性介导血管活性剂的合成和/或释放。在这篇文章中，我们讨论了COX 2的抑制减少PG的合成，并通过防止伤害感受器的敏化而产生有益的作用，但同时，它可能通过损害血管活性剂的合成和/或释放而导致有害的心血管效应。
Prostaglandins (PGs) are requisite components of inflammatory pain as indicated by the efficacy of cyclooxygenase 1/2 (COX1/2) inhibitors. PGs do not activate nociceptive ion channels directly, but sensitize them by downstream mechanisms linked to G-protein coupled receptors. Antiinflammatory effects are purported to arise from inhibition of synthesis and/or release of proinflammatory agents. Release of these agents from peripheral and central terminals of sensory neurons modulates nociceptive input from the periphery and synaptic transmission at the first sensory synapse, respectively. Heart and blood vessels are densely innervated by sensory nerve endings that express chemo-, mechano-, and thermo-sensitive receptors. Activation of these receptors mediates synthesis and/or release of vasoactive agents by virtue of their Ca2+permeability. In this article, we discuss that inhibition of COX2 reduces PG synthesis and renders beneficial effects by preventing sensitization of nociceptors, but at the same time, it might contribute to deleterious cardiovascular effects by compromising the synthesis and/or release of vasoactive agents.
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