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



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



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.

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Accession: 006351220

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