Abstract
Membrane potential is a principal regulator of arterial contractility. Arterial smooth muscle cells express several different types of ion channel that control membrane potential, including K(V) channels. K(V) channel activation leads to membrane hyperpolarization, resulting in inhibition of voltage-dependent Ca(2+) channels, a reduction in [Ca(2+) ](i) , and vasodilation. In contrast, K(V) channel inhibition leads to membrane depolarization and vasoconstriction. The ability of K(V) channels to regulate arterial contractility is dependent upon the number of plasma membrane-resident channels and their open probability. Here, we will discuss mechanisms that alter the surface abundance of K(V) channel proteins in arterial smooth muscle cells and the functional consequences of such regulation. Cellular processes that will be described include those that modulate K(V) channel transcription, retrograde and anterograde trafficking, and protein degradation.