Lactate enhances the acid-sensing Na+ channel on ischemia-sensing neurons
Lactate enhances the acid-sensing Na+ channel on ischemia-sensing neurons
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DOI：
10.1038/nn0901-869
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发表时间：
2001-09-01
影响因子：
25
通讯作者：
McCleskey, EW
中科院分区：
文献类型：
--
作者：
Immke, DC;McCleskey, EW
心肌缺血时由无氧代谢产生的乳酸是引发心绞痛性胸痛的几种化合物之一1,2；然而，当冠状动脉闭塞时达到的pH值（pH 7.0至6.7）3,4也可能发生在全身性酸中毒中，这不会引起胸痛。在这里，我们发现乳酸通过细胞外二价离子作用，显著增加酸敏感离子通道（ASIC）的活性，该通道在支配心脏的感觉神经元上高度表达5,6。与全身性病理引起的酸中毒相比，表达asic的神经元对局部缺血的乳酸酸中毒具有额外的敏感性。
Lactic acid produced by anaerobic metabolism during cardiac ischemia is among several compounds suggested to trigger anginal chest pain 1, 2; however, the pH reached when a coronary artery is occluded (pH 7.0 to 6.7) 3, 4 can also occur during systemic acidosis, which causes no chest pain. Here we show that lactate, acting through extracellular divalent ions, dramatically increases activity of an acid-sensing ion channel (ASIC) that is highly expressed on sensory neurons that innervate the heart 5, 6. The effect should confer upon neurons that express ASICs an extra sensitivity to the lactic acidosis of local ischemia compared to acidity caused by systemic pathology.