Hypoxia-induced modulation of O₂-sensitive K⁺ channels in pulmonary vascular smooth muscle cells

The regulation of ion channel activity is key to the maintenance of cellular excitability in many cell types. In vascular smooth muscle, the activity of K+ channels is essential to the control of membrane excitability in that K+ channels are responsible for setting the resting membrane potential (RMP) at relatively negative membrane potentials (1). Alteration of K+ channel activity or gene expression will therefore have a major impact on cell excitability. Indeed, dysfunctional ion channels permeable to K+, Na+, Ca2+, and Cl have been involved in many forms of cardiovascular disease (2-5).