Voltage-gated potassium channels in pulmonary artery smooth muscle cells

In most electrically excitable cells, voltage-gated potassium (Kv) channels play an important role in determining the magnitude and duration of the action potential. Differences in the type(s) and=or levels of K+ channel expression contribute to the heterogeneity of action potential regulation. However, in pulmonary artery vascular smooth muscle cells (VSMCs), Kv channels play a central role in establishing the resting membrane potential as opposed to regulating the action potential. Closure of VSMC K+ channels, open at the resting membrane potential, causes membrane depolarization. This change in membrane potential activates voltage-gated Ca2+ channels, leading to an increase in intracellular calcium concentration and vasoconstriction (1). Activation of VSMC K+ channels leads to hyperpolarization, inhibition of voltage-gated Ca2+ channels, and vasodilation (1). Vascular smooth muscle cells have a high input resistance; therefore, even a small change in K+ channel activity can have a significant effect on membrane potential and consequently on vascular tone (2,3). Indeed, many factors that modulate vessel tone do so by activating or inhibiting VSMC K+ channels (1).