Beta-adrenergic inhibition of cardiac sodium channels by dual G-protein pathways.
Beta-adrenergic inhibition of cardiac sodium channels by dual G-protein pathways.
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通过双重 G 蛋白途径抑制心脏钠通道的 β 肾上腺素能。
DOI：
10.1126/science.2547248
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Brown,AM
中科院分区：
文献类型：
--
作者：
Schubert,B;VanDongen,AM;Kirsch,GE;Brown,AM
β肾上腺素能激动剂调节电压依赖性心肌钠电流的信号通路尚不清楚，但可能与腺苷3‘5’-单磷酸(CAMP)有关。在心肌细胞上测量了单通道和全细胞钠电流，并发现信号转导G蛋白GS通过细胞质(间接)和膜分隔(直接)途径将β-肾上腺素能受体偶联到钠通道。因此，Gcan至少作用于心脏中的三个效应器：钠通道、钙通道和腺苷环化酶。膜去极化对钠电流的作用是抑制的，而对钠电流的作用则增强。在心肌缺血期间，去极化细胞的钠电流可能会被伴随的儿茶酚胺水平的增加而进一步抑制。
The signaling pathways by which β-adrenergic agonists modulate voltage-dependent cardiac sodium currents are unknown, although it is likely that adenosine 3′5′-monophosphate (cAMP) is involved. Single-channel and whole-cell sodium currents were measured in cardiac myocytes and the signal transducing G protein Gswas found to couple β-adrenergic receptors to sodium channels by both cytoplasmic (indirect) and membrane-delimited (direct) pathways. Hence, Gscan act on at least three effectors in the heart: sodium channels, calcium channels, and adenylyl cyclase. The effect on sodium currents was inhibitory and was enhanced by membrane depolarization. During myocardial ischemia the sodium currents of depolarized cells may be further inhibited by the accompanying increase in catecholamine levels.