ABSTRACT

Membrane ion channels play an essential role in the maintenance of cellular excitability. In vascular smooth muscle, membrane excitability is principally controlled by voltage-gated Kþ channels, which are responsible for setting the resting membrane potential (1). Changes in Kþ channel function can profoundly affect vascular tone by regulating voltage-gated Ca2þ channel function; an increase in Kþ conductance hyperpolarizes the membrane, inhibiting the activation of Ca2þ channels, whereas a decrease in Kþ conductance results in depolarization and the subsequent activation of voltage-gated Ca2þ channels (1). The role of Kþ channel function in regulating PASMC contraction is summarized in Fig. 1.