NDLI: T-tubule localization of the inward-rectifier K+ channel in mouse ventricular myocytes: a role in K+ accumulation

Content Provider	PubMed Central
Author	Clark, Robert B. Tremblay, Annie Melnyk, Peter Allen, Bruce G. Giles, Wayne R. Fiset, Céline
Copyright Year	2001
Abstract	The properties of the slow inward ‘tail currents’ (I tail) that followed depolarizing steps in voltage-clamped, isolated mouse ventricular myocytes were examined. Depolarizing steps that produced large outward K+ currents in these myocytes were followed by a slowly decaying inward I tail on repolarization to the holding potential. These currents were produced only by depolarizations: inwardly rectifying K+ currents, I K1, produced by steps to potentials negative to the holding potential, were not followed by I tail. For depolarizations of equal duration, the magnitude of I tail increased as the magnitude of outward current at the end of the depolarizing step increased. The apparent reversal potential of I tail was dependent upon the duration of the depolarizing step, and the reversal potential shifted to more depolarized potentials as the duration of the depolarization was increased. Removal of external Na+ and Ca2+ had no significant effect on the magnitude or time course of I tail. BaCl2 (0.25 mm), which had no effect on the magnitude of outward currents, abolished I tail and I K1 simultaneously. Accordingly, I tail in mouse ventricular myocytes probably results from K+ accumulation in a restricted extracellular space such as the transverse tubule system (t-tubules). The efflux of K+ into the t-tubules during outward currents produced by depolarization shifts the K+ Nernst potential (E K) from its ‘resting’ value (close to −80 mV) to more depolarized potentials. This suggests that I tail is produced by I K1 in the t-tubules and is inward because of the transiently elevated K+ concentration and depolarized value of E K in the t-tubules. Additional evidence for the localization of I K1 channels in the t-tubules was provided by confocal microscopy using a specific antibody against Kir2.1 in mouse ventricular myocytes.
Related Links	http://dx.doi.org/10.1111/j.1469-7793.2001.00979.x
Ending Page	992
Page Count	14
Starting Page	979
File Format	PDF
ISSN	00223751
e-ISSN	14697793
Journal	The Journal of Physiology
Issue Number	Pt 3
Volume Number	537
Language	English
Publisher	Blackwell Science Inc
Publisher Date	2001-12-15
Access Restriction	Open
Rights Holder	Blackwell Science Inc
Subject Keyword	Physiology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Physiology Sports Science

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