Regulation of Adenosine-activated GIRK Channels by Gq-coupled Receptors in Mouse Atrial Myocytes.

The Korean Journal of Physiology & Pharmacology : Official Journal of the Korean Physiological Society and the Korean Society of Pharmacology
Hana Cho

Abstract

Adenosine (Ado) is an important mediator of the endogenous defense against ischemia-induced injury in the heart. The action of Ado is mediated by activation of G protein-gated inwardly rectifying K(+) (GIRK) channels. In turn, GIRK channels are inhibited by reducing phosphatidylinositol 4,5-bisphosphate (PIP(2)) through Gq protein-coupled receptors (GqPCRs). We previously found that GIRK channels activated by acetylcholine, a muscarinic M2 acetylcholine receptor agonist, are inhibited by GqPCRs in a receptor-specific manner. However, it is not known whether GIRK channels activated by Ado signaling are also regulated by GqPCRs. Presently, this was investigated in mouse atrial myocytes using the patch clamp technique. GIRK channels were activated by 100 microM Ado. When Ado was repetitively applied at intervals of 5~6 min, the amplitude of second Ado-activated GIRK currents (I(K(Ado))) was 88.3+/-3.7% of the first I(K(Ado)) in the control. Pretreatment of atrial myocytes with phenylephrine, endothelin-1, or bradykinin prior to a second application of Ado reduced the amplitude of the second I(K(Ado)) to 25.5+/-11.6%, 30.5+/-5.6%, and 96.0+/-2.7%, respectively. The potency of I(K(Ado)) inhibition by GqPCRs was different with that o...Continue Reading

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Citations

Jun 10, 2020·Proceedings of the National Academy of Sciences of the United States of America·Allison AndersonKevin Wickman
Sep 17, 2019·Cellular Signalling·Anne NiemeyerMarie-Cecile Kienitz

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