Generation of a constitutive Na+-dependent inward-rectifier current in rat adult atrial myocytes by overexpression of Kir3.4.

Generation of a constitutive Na+-dependent inward-rectifier current in rat adult atrial myocytes by overexpression of Kir3.4. Research Abstract Details 

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Generation of a constitutive Na+-dependent inward-rectifier current in rat adult atrial myocytes by overexpression of Kir3.4. Abstract Text:

Elisa Mintert,Leif I ,Andreas Rinne,Mathias Timpert, Kienitz,Lutz Pott,Kirsten Bender,Elisa Mintert,Leif I ,Andreas Rinne,Mathias Timpert, Kienitz,Lutz Pott,Kirsten Bender,

Apart from gating by interaction with betagamma subunits from heterotrimeric G proteins upon stimulation of appropriate receptors, Kir.3 channels have been shown to be gated by intracellular Na(+). However, no information is available on how Na(+)-dependent gating affects endogenous Kir3.1/Kir3.4 channels in mammalian atrial myocytes. We therefore studied how loading of adult atrial myocytes from rat hearts via the patch pipette filling solution with different concentrations of Na(+) ([Na(+)](pip)) affects Kir3 current. Surprisingly, in a range between 0 and 60 mm, Na(+) neither had an effect on basal inward-rectifier current nor on the current activated by acetylcholine. Overexpression of Kir3.4 in adult atrial myocytes forced by adenoviral gene transfer results in formation of functional homomeric channels that interact with betagamma subunits upon activation of endogenous muscarinic receptors. These channels are activated at [Na(+)](pip) >/= 15 mm, resulting in a receptor-independent basal inward rectifier current (I(bir)). I(bir) was neither affected by pertussis toxin nor by GDP-beta-S, suggesting G-protein-independent activation. PIP(2) depletion via endogenous PLC-coupled alpha(1) adrenergic receptors causes inhibition of endogenous Kir3.1/3.4 channel currents by about 75%. In contrast, inhibition of Na(+)-activated I(bir) amounts to < 20%. The effect of the Kir3 channel blocker tertiapin-Q can be described using an IC(50) of 12 nm (endogenous I(K(ACh))) and 0.61 nm (I(bir)). These data clearly identify I(bir) as a homotetrameric Kir3.4 channel current with novel properties of regulation and pharmacology. I(bir) shares some properties with a basal current recently described in atrial myocytes from an animal model of atrial fibrillation (AF) and AF patients.

Generation of a constitutive Na+-dependent inward-rectifier current in rat adult atrial myocytes by overexpression of Kir3.4. Publishing Authors By Initials

E Mintert,LI ,A Rinne,M Timpert,MC Kienitz,L Pott,K Bender,E Mintert,LI ,A Rinne,M Timpert,MC Kienitz,L Pott,K Bender,

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Generation of a constitutive Na+-dependent inward-rectifier current in rat adult atrial myocytes by overexpression of Kir3.4. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: The Journal of physiology

VOLUME: 585

Page Numbers: 3-13

Journal Abbreviation: J. Physiol. (Lond.)

ISSN: 0022-3751

DAY: 20

MONTH: 09

YEAR: 2007

Generation of a constitutive Na+-dependent inward-rectifier current in rat adult atrial myocytes by overexpression of Kir3.4. Information

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LANGUAGE: eng

NlmUniqueID: 266262

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Grant and Affiliation Information for Generation of a constitutive Na+-dependent inward-rectifier current in rat adult atrial myocytes by overexpression of Kir3.4.

AFFILIATION: Institute of Physiology, Ruhr-University Bochum, D 44780 Bochum, Germany. lutz.pott@rub.de.

Country: England

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MEDLINETA: J Physiol

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