Shim A L, Mitrokhin V M, Kazanski V E, Mladenov M I, Kamkin A G
Department of Physiology, N. I. Pirogov Russian National Research Medical University, Ministry of Health of the Russian Federation, Moscow, Russia.
Bull Exp Biol Med. 2017 Oct;163(6):705-709. doi: 10.1007/s10517-017-3885-9. Epub 2017 Oct 23.
Depolarization of cardiomyocytes triggered by stretch and activation of mechanically gated ion channels can lead to serious arrhythmias. However, stretch-induced signaling activating these channels remain little studied. This study tested the hypothesis on implication of NO in shaping the electrical abnormalities provoked by stretch of the right atrial myocardium in rat via a mechanism engaging a signaling cascade, where NO plays a significant role. This approach showed that in isolated right atrial preparation, NO donor SNAP induces the electrical abnormalities similar to those provoked by stretch, and the latter results from activation of NO synthase.
由拉伸和机械门控离子通道激活引发的心肌细胞去极化可导致严重心律失常。然而,激活这些通道的拉伸诱导信号传导仍鲜为人知。本研究通过一种涉及信号级联反应的机制,验证了一氧化氮(NO)在塑造大鼠右心房心肌拉伸引发的电异常中的作用这一假设,其中NO发挥着重要作用。该方法表明,在离体右心房标本中,NO供体硝普钠(SNAP)可诱导出与拉伸引发的电异常相似的情况,且后者是由一氧化氮合酶激活所致。