Schubert B, VanDongen A M, Kirsch G E, Brown A M
Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX 77030.
Science. 1989 Aug 4;245(4917):516-9. doi: 10.1126/science.2547248.
The signaling pathways by which beta-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 Gs was found to couple beta-adrenergic receptors to sodium channels by both cytoplasmic (indirect) and membrane-delimited (direct) pathways. Hence, Gs can 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.
β-肾上腺素能激动剂调节电压依赖性心脏钠电流的信号通路尚不清楚，尽管很可能涉及3',5'-环磷酸腺苷（cAMP）。在心肌细胞中测量了单通道和全细胞钠电流，发现信号转导G蛋白Gs通过细胞质（间接）和膜限定（直接）途径将β-肾上腺素能受体与钠通道偶联。因此，Gs可作用于心脏中的至少三种效应器：钠通道、钙通道和腺苷酸环化酶。对钠电流的影响是抑制性的，并且通过膜去极化增强。在心肌缺血期间，去极化细胞的钠电流可能会因儿茶酚胺水平的伴随升高而进一步受到抑制。
