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

Andre Terzic, Robert T. Tung, Atsushi Inanobe, Toshiaki Katada, Yoshihisa Kurachi

Research output: Contribution to journalArticle

73 Scopus citations

Abstract

To determine whether G proteins activate cardiac ATP-sensitive K+ (KATP) channels by regulating intracellular ATP (ATPi)-dependent gating, currents were measured in inside-out patches. When ATPi closed KATP channels, activators of endogenous G proteins, GTP (plus adenosine or acetylcholine), GTPγS, or AIF4- stimulated channels, an effect prevented by GDPβS. In the absence of ATPi, G protein activators were ineffective. Intracellular nucleoside diphosphates restored KATP channel openings after the "rundown" of spontaneous activity. Only when ATPi suppressed nucleoside diphosphate-induced openings, GTPγS or AIF4- enhanced KATP channel activity. Active forms of exogenous G protein subunits (Gαi-1, Gαi-2, or Gα0 activated only KATP channels closed by ATPi. G proteins stimulate cardiac KATP channels apparently by antagonizing ATPi-dependent inhibitory gating. Regulation of ligand-dependent gating represents a distinct type of G protein modulation of ion channels.

Original languageEnglish (US)
Pages (from-to)885-893
Number of pages9
JournalNeuron
Volume12
Issue number4
DOIs
StatePublished - Apr 1994

ASJC Scopus subject areas

  • Neuroscience(all)

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