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Role of intracellular magnesium in the activation of muscarinic potassium channel in cardiac atrial cell membrane


Pfluegers Archiv European Journal of Physiology 407(5): 572-574
Role of intracellular magnesium in the activation of muscarinic potassium 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 recording, 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 protomer of pertussi toxin with NAD. From these observations, we concluded: 1) Intracellular Mg2+ is essential for GTP to activate the GTP-binding protein. 2) Deactivation of the N protein may be caused by hydrolysis of GTP to GDP. This process may not require Mg2+. 3) During the activation by GTP analogues, the N protein may be dissociated into its subunits.


Accession: 006351220



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