Role of intracellular Mg2+ in the activation of muscarinic K+ channel in cardiac atrial cell membrane.
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.
D000818:Animals; D002462:Cell Membrane / Q000378:metabolism; D003584:Cytological Techniques; D004594:Electrophysiology; D019204:GTP-Binding Proteins / Q000502:physiology; D006160:Guanosine Triphosphate / Q000378:metabolism / Q000494:pharmacology; D006168:Guinea Pigs; D006325:Heart Atria / Q000166:cytology / Q000378:metabolism*; D066298:In Vitro Techniques; D007473:Ion Channels / Q000187:drug effects / Q000378:metabolism*; D008274:Magnesium / Q000494:pharmacology / Q000502:physiology*; D008564:Membrane Potentials; D011188:Potassium / Q000378:metabolism*; D011976:Receptors, Muscarinic / Q000502:physiology*
D007473:Ion Channels; D011976:Receptors, Muscarinic; D006160:Guanosine Triphosphate; D019204:GTP-Binding Proteins; D008274:Magnesium; D011188:Potassium