Plasticity of KIR channels in human smooth muscle cells from internal thoracic artery.
Inwardly rectifying K(+) (K(IR)) 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 Ba(2+). 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). Ba(2+) depolarized all cells, whereas small increases in extracellular K(+) concentration elicited hyperpolarization only in contractile cells. Ba(2+) inhibited [(3)H]thymidine incorporation, indicating a possible role for K(IR) channels in the regulation of proliferation. The phenotype-dependent plasticity of K(IR) channels may have relevance to vascular remodeling.[1]References
- Plasticity of KIR channels in human smooth muscle cells from internal thoracic artery. Karkanis, T., Li, S., Pickering, J.G., Sims, S.M. Am. J. Physiol. Heart Circ. Physiol. (2003) [Pubmed]
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