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Am J Physiol Heart Circ Physiol 284: H2325-H2334, 2003. First published February 21, 2003; doi:10.1152/ajpheart.00559.2002
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Vol. 284, Issue 6, H2325-H2334, June 2003

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

Tom Karkanis1, Shaohua Li2,3, J. Geoffrey Pickering2,3, and Stephen M. Sims1

Departments of 1 Physiology and Pharmacology and 2 Medicine and 3 Robarts Research Institute, University of Western Ontario, London, Ontario, Canada N6A 5C1

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 a large inward current that was selective for K+ and blocked by Ba2+. Current density was greater in proliferative compared with contractile cells (-4.5 ± 0.9 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, whereas 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.

ion channels; electrophysiology; inward rectifier; proliferation


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