Abstract

See related article, pages 1280–1287 Potassium channels play a major role in the immediate and long term regulation of vascular smooth muscle function.1 The activity of these ion channels determines and regulates cell membrane potential, which, in turn, regulates the open state probability of voltage-gated Ca2+ channels, Ca2+ influx, and intracellular Ca2+. The concentration of intracellular Ca2+ not only regulates the immediate contractile responses of smooth muscle cells (ie, vascular tone),1 but also the long term responses of these cells through control of gene expression.2 By their effect on membrane potential, K+ channels also establish the electrochemical gradient that determines the movement of other ions across the plasma membrane. In addition, potassium channels participate significantly in cell volume regulation.3 Over the past two decades it has become apparent that K+ channels also play an important role in cell proliferation.4–8 In vascular smooth muscle cells, investigators have identified increased expression of intermediate conductance, Ca2+-activated K+ (IKCa) channels (KCa3.1, locus: KCNN4) associated with proliferation,4 and recent studies have shown that selective inhibition of these channels prevents vascular smooth muscle proliferation associated with injury-induced restenosis.9 The study by Miguel-Velado et al in this issue of Circulation Research 10 confirms …

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.