K_V channel trafficking and control of vascular tone

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 Ca²⁺ channels, a reduction in [Ca²⁺ ]_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.