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Am J Physiol Heart Circ Physiol (February 21, 2003). doi:10.1152/ajpheart.00559.2002
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Submitted on July 3, 2002
Accepted on February 19, 2003

Plasticity of KIR channels in human smooth muscle cells from the internal thoracic artery

Tom Karkanis1, Shaohua Li2, J. G. Pickering2, and Stephen M. Sims1*

1 Departments of Physiology and Pharmacology, University of Western Ontario, London, Ontario, Canada
2 Department of Medicine, University of Western Ontario, London, Ontario, Canada

* To whom correspondence should be addressed. E-mail: stephen.sims{at}fmd.uwo.ca.

Inwardly rectifying K+ (KIR ) currents are present in some, but not all, vascular smooth muscles. We used patch-clamp methods to examine plasticity of this current by comparing contractile and proliferative phenotypes of a clonal human vascular smooth muscle cell line. Hyperpolarization of cells under voltage clamp elicited large inward current which was selective for K+ and blocked by Ba2+. Current density was greater in proliferative compared to contractile cells (-4.5±0.9 pA/pF and -1.4±0.3 pA/pF, respectively; P<0.001). RT-PCR of mRNA from proliferative cells identified transcripts for Kir2.1 and Kir2.2 but not Kir2.3 potassium channels. Western blot analysis demonstrated greater expression of Kir2.1 protein in proliferative cells, consistent with the higher current density. Proliferative cells displayed a more negative membrane potential than contractile cells (-71±2 and -35±4 mV, respectively; P<0.001). Ba2+ depolarized all cells, while small increases in extracellular K+ concentration elicited hyperpolarization only in contractile cells. Ba2+ inhibited [3H]-thymidine incorporation, indicating a possible role for Kir channels in the regulation of proliferation. The phenotype-dependent plasticity of Kir channels may have relevance to vascular remodeling.




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