Ion Channel Trafficking in Arterial Smooth Muscle Cells and Functional Significance

Many different ion channels control arterial smooth muscle cell contractility. Physiological and pathological stimuli and their downstream signaling processes can regulate ion channel function through transcriptional modulation and post-translational modification of protein subunits. Although the cellular current generated by ion channels is equally dependent upon number of channels and open probability, it has only recently been demonstrated that physiological and pathological stimuli control the number of surface channel proteins in arterial smooth muscle cells. Voltage-gated Ca²⁺ channels couple membrane potential to Ca²⁺ influx in arterial smooth muscle. K_V channels can form either homo- or hetero-tetramers, including in arterial smooth muscle cells, leading to diverse K⁺ current phenotypes. Arterial smooth muscle cells express transient receptor potential (TRP) channels from several different families. TRP channel trafficking has primarily been investigated using recombinant proteins and non-vascular cells. TRP family of non-selective cation channels comprises 28 distinct proteins in mammals.