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延长的动作电位和后去极化并非由于一氧化氮合酶3基因敲除心室肌细胞中钾电流的变化所致。

Prolonged Action Potential and After depolarizations Are Not due to Changes in Potassium Currents in NOS3 Knockout Ventricular Myocytes.

作者信息

Wang Honglan, Bonilla Ingrid M, Huang Xin, He Quanhua, Kohr Mark J, Carnes Cynthia A, Ziolo Mark T

机构信息

Department of Physiology and Cell Biology, The Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, OH 43221, USA.

出版信息

J Signal Transduct. 2012;2012:645721. doi: 10.1155/2012/645721. Epub 2012 Aug 28.

DOI:10.1155/2012/645721
PMID:22970362
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3434404/
Abstract

Ventricular myocytes deficient in endothelial nitric oxide synthase (NOS3(-/-)) exhibit prolonged action potential (AP) duration and enhanced spontaneous activity (early and delayed afterdepolarizations) during β-adrenergic (β-AR) stimulation. Studies have shown that nitric oxide is able to regulate various K(+) channels. Our objective was to examine if NOS3(-/-) myocytes had altered K(+) currents. APs, transient outward (I(to)), sustained (I(Ksus)), and inward rectifier (I(K1)) K(+) currents were measured in NOS3(-/-) and wild-type (WT) myocytes. During β-AR stimulation, AP duration (measured as 90% repolarization-APD(90)) was prolonged in NOS3(-/-) compared to WT myocytes. Nevertheless, we did not observe differences in I(to), I(Ksus), or I(K1) between WT and NOS3(-/-) myocytes. Our previous work showed that NOS3(-/-) myocytes had a greater Ca(2+) influx via L-type Ca(2+) channels with β-AR stimulation. Thus, we measured β-AR-stimulated SR Ca(2+) load and found a greater increase in NOS3(-/-) versus WT myocytes. Hence, our data suggest that the prolonged AP in NOS3(-/-) myocytes is not due to changes in I(to), I(Ksus), or I(K1). Furthermore, the increase in spontaneous activity in NOS3(-/-) myocytes may be due to a greater increase in SR Ca(2+) load. This may have important implications for heart failure patients, where arrhythmias are increased and NOS3 expression is decreased.

摘要

内皮型一氧化氮合酶缺乏（NOS3(-/-)）的心室肌细胞在β-肾上腺素能（β-AR）刺激期间表现出动作电位（AP）时程延长和自发活动增强（早期和延迟后去极化）。研究表明，一氧化氮能够调节各种钾离子通道。我们的目的是研究NOS3(-/-)肌细胞的钾离子电流是否发生改变。在NOS3(-/-)和野生型（WT）肌细胞中测量了动作电位、瞬时外向（I(to)）、持续（I(Ksus)）和内向整流（I(K1)）钾离子电流。在β-AR刺激期间，与WT肌细胞相比，NOS3(-/-)肌细胞的动作电位时程（以90%复极化-APD(90)测量）延长。然而，我们未观察到WT和NOS3(-/-)肌细胞在I(to)、I(Ksus)或I(K1)方面存在差异。我们之前的工作表明，在β-AR刺激下，NOS3(-/-)肌细胞通过L型钙通道有更大的钙内流。因此，我们测量了β-AR刺激下的肌浆网钙负荷，发现与WT肌细胞相比，NOS3(-/-)肌细胞的增加幅度更大。因此，我们的数据表明，NOS3(-/-)肌细胞中动作电位延长并非由于I(to)、I(Ksus)或I(K1)的变化。此外，NOS3(-/-)肌细胞中自发活动的增加可能是由于肌浆网钙负荷的更大增加。这可能对心力衰竭患者具有重要意义，这些患者心律失常增加且NOS3表达降低。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e649/3434404/cd52dbb41139/JST2012-645721.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e649/3434404/2e4cb42d8893/JST2012-645721.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e649/3434404/ce319e80ec5b/JST2012-645721.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e649/3434404/b05e746c2b4c/JST2012-645721.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e649/3434404/cd52dbb41139/JST2012-645721.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e649/3434404/2e4cb42d8893/JST2012-645721.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e649/3434404/ce319e80ec5b/JST2012-645721.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e649/3434404/b05e746c2b4c/JST2012-645721.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e649/3434404/cd52dbb41139/JST2012-645721.004.jpg

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