ABSTRACT
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 Kþ 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 Kþ channels, open at the resting membrane potential, causes membrane depolarization. This change in membrane potential activates voltage-gated Ca2þ
channels, leading to an increase in intracellular calcium concentration and vasoconstriction (1). Activation of VSMC Kþ channels leads to hyperpolarization, inhibition of voltage-gated Ca2þ channels, and vasodilation (1). Vascular smooth muscle cells have a high input resistance; therefore, even a small change in Kþ 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 Kþ channels (1).
