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Related Experiment Videos

G proteins activate ATP-sensitive K+ channels by antagonizing ATP-dependent gating

A Terzic1, R T Tung, A Inanobe

  • 1Department of Internal Medicine, Mayo Clinic, Rochester, Minnesota 55905.

Neuron
|April 1, 1994
PubMed
Summary

G proteins activate cardiac ATP-sensitive potassium (KATP) channels by counteracting the inhibitory effects of intracellular ATP. This G protein modulation of KATP channel gating is distinct from other known mechanisms.

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Area of Science:

  • Molecular and Cellular Biology
  • Cardiovascular Physiology
  • Ion Channel Function

Background:

  • Cardiac ATP-sensitive potassium (KATP) channels play a crucial role in regulating cardiac function and energy balance.
  • G protein signaling pathways are known to influence various cellular processes, including ion channel activity.

Purpose of the Study:

  • To investigate the mechanism by which G proteins modulate the activity of cardiac ATP-sensitive potassium (KATP) channels.
  • To determine if G proteins regulate KATP channels by affecting intracellular ATP (ATPi)-dependent gating.

Main Methods:

  • Utilized inside-out patch-clamp electrophysiology to measure KATP channel currents in cardiac cells.
  • Applied activators and inhibitors of G proteins (GTP, GTPγS, AlF⁻⁴, GDPβS) and varied intracellular ATP concentrations.

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  • Tested the effects of active G protein subunits (Gαi-1, Gαi-2, Gαo) on KATP channel activity.

    • Main Results:

    • G protein activators stimulated KATP channels only when intracellular ATP (ATPi) was present and closed the channels.
    • G protein activation was ineffective in the absence of ATPi, and GDPβS prevented G protein-mediated channel stimulation.
    • Active G protein subunits specifically activated KATP channels that were inhibited by ATPi, suggesting antagonism of ATPi-dependent gating.

    Conclusions:

    • G proteins stimulate cardiac KATP channels primarily by antagonizing the inhibitory effects of intracellular ATP (ATPi).
    • This represents a novel mechanism of G protein modulation, distinct from regulation of ligand-dependent gating.
    • Understanding this interaction is key to comprehending cardiac electrophysiology and energy metabolism regulation.