G protein-independent inhibition of GIRK current by adenosine in rat atrial myocytes overexpressing A1 receptors after adenovirus-mediated gene transfer.

@article{Bsche2003GPI,
  title={G protein-independent inhibition of GIRK current by adenosine in rat atrial myocytes overexpressing A1 receptors after adenovirus-mediated gene transfer.},
  author={Leif Ilja B{\"o}sche and Marie-C{\'e}cile Wellner-Kienitz and Kirsten Bender and Lutz Pott},
  journal={The Journal of physiology},
  year={2003},
  volume={550 Pt 3},
  pages={707-17}
}
G protein-activated inwardly rectifying K+ (GIRK) channels, important regulators of membrane excitability in the heart and central nervous system, are activated by interaction with betagamma subunits from heterotrimeric G proteins upon receptor stimulation. In atrial myocytes various endogenous receptors couple to GIRK channels, including the canonical muscarinic M2 receptor (M2AChR) and the A1 adenosine receptor (A1AdoR). Saturating stimulation of A1AdoR in atrial myocytes activates only a… CONTINUE READING