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This Article Full Text Full Text (PDF) All Versions of this Article: 568/3/749    most recent jphysiol.2005.085746v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Makary, S. M. Y Articles by Boyett, M. R Search for Related Content PubMed PubMed Citation Articles by Makary, S. M. Y Articles by Boyett, M. R

¹ Division of Cardiovascular and Endocrine Sciences, University of Manchester, Manchester Incubator Building, 48 Grafton Street, Manchester M13 9XX, UK
² Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA

Inward rectification is caused by voltage-dependent block of the channel pore by intracellular Mg²⁺ and polyamines such as spermine. In the present study, we compared inward rectification in the Kir3.1/Kir3.4 channel, which underlies the cardiac current I_K,ACh, and the Kir2.1 channel, which underlies the cardiac current I_K,1. Sustained outward current at potentials positive to the K⁺ reversal potential was observed through Kir3.1/Kir3.4, but not Kir2.1, demonstrating that Kir3.1/Kir3.4 exhibits weaker inward rectification than Kir2.1. We show that Kir3.1/Kir3.4 is more sensitive to extracellular spermine block than Kir2.1, and that intracellular and extracellular polyamines can permeate Kir3.1/Kir3.4, but not Kir2.1, to a limited extent. We describe a simple kinetic model in which polyamines act as permeant blockers of Kir3.1/Kir3.4, but as relatively impermeant blockers of Kir2.1. The model shows the difference in sensitivity to extracellular spermine block, as well as the difference in the extent of inward rectification between the two channels. This suggests that Kir3.1/Kir3.4 exhibits weaker inward rectification than Kir2.1 because of the difference in the balance of polyamine block and permeation of the two channels.

(Received 24 February 2005; accepted after revision 16 August 2005; first published online 18 August 2005)
Corresponding author M. R. Boyett: Division of Cardiovascular and Endocrine Sciences, University of Manchester, Manchester Incubator Building, 48 Grafton Street, Manchester M13 9XX, UK. Email: mark.boyett{at}manchester.ac.uk

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