Role of intracellular Mg2+ in the activation of muscarinic K+ channel in cardiac atrial cell membrane

Pflugers Arch. 1986 Nov;407(5):572-4. doi: 10.1007/BF00657521.


Effects of intracellular Mg2+ in the activation of a muscarinic K+ channel were examined in single atrial cells, using patch-recording techniques. In "cell-attached" patch recordings, acetylcholine (ACh) or adenosine (Ado), present in the pipette, activated a specific population of K+ channels. In "inside-out" patches, openings of the K+ channel by ACh or Ado diminished and did not resume until Mg2+ was added to the perfusate which contained GTP or GTP-gamma S, a non-hydrolyzable GTP analogue. Channel openings caused by GTP faded by removing Mg2+, while GTP-gamma S-induced openings persisted steadily even when both Mg2+ and GTP-gamma S were removed. In contrast to the case of GTP-induced channel openings, the GTP-gamma S-induced openings were not inhibited by the A promoter of pertussis toxin with NAD. From these observations, we concluded: Intracellular Mg2+ is essential for GTP to activate the GTP-binding protein. Deactivation of the N protein may be caused by hydrolysis of GTP to GDP. This process may not require Mg2+. During the activation by GTP analogues, the N protein may be dissociated into its subunits.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Membrane / metabolism
  • Cytological Techniques
  • Electrophysiology
  • GTP-Binding Proteins / physiology
  • Guanosine Triphosphate / metabolism
  • Guanosine Triphosphate / pharmacology
  • Guinea Pigs
  • Heart Atria / cytology
  • Heart Atria / metabolism*
  • In Vitro Techniques
  • Ion Channels / drug effects
  • Ion Channels / metabolism*
  • Magnesium / pharmacology
  • Magnesium / physiology*
  • Membrane Potentials
  • Potassium / metabolism*
  • Receptors, Muscarinic / physiology*


  • Ion Channels
  • Receptors, Muscarinic
  • Guanosine Triphosphate
  • GTP-Binding Proteins
  • Magnesium
  • Potassium