Beta-adrenergic inhibition of cardiac sodium channels by dual G-protein pathways.

Journal Article (Journal Article)

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.

Full Text

Duke Authors

Cited Authors

  • Schubert, B; VanDongen, AM; Kirsch, GE; Brown, AM

Published Date

  • August 4, 1989

Published In

Volume / Issue

  • 245 / 4917

Start / End Page

  • 516 - 519

PubMed ID

  • 2547248

International Standard Serial Number (ISSN)

  • 0036-8075

Digital Object Identifier (DOI)

  • 10.1126/science.2547248


  • eng

Conference Location

  • United States