Smooth muscle myosin light chain kinase (MLCK) plays a crucial role in artery contraction, which regulates blood pressure and blood flow distribution. In addition to this role, MLCK contributes to Ca(2+) flux regulation in vascular smooth muscle (VSM) and in non-muscle cells, where cytoskeleton has been suggested to help Ca(2+) channels trafficking. This conclusion is based on the use of pharmacological inhibitors of MLCK and molecular and cellular techniques developed to down-regulate the enzyme. Dissimilarities have been observed between cells and whole tissues, as well as between large conductance and small resistance arteries. A differential expression in MLCK and ion channels (either voltage-dependent Ca(2+) channels or non-selective cationic channels) could account for these observations, and is in line with the functional properties of the arteries. A potential involvement of MLCK in the pathways modulating Ca(2+) entry in VSM is described in the present review.
Keywords: CaM, calmodulin; ER, endoplasmic reticulum; MLCK, myosin light chain kinase; Myosin light chain kinase; ROC, receptor-operated Ca2+ (channel); SMC, smooth muscle cell; SOC, store-operated Ca2+ (channel); SR, sarcoplasmic reticulum; TRP; TRP, transient receptor potential (channel); VOC, voltage-operated Ca2+ (channel); VSM, vascular smooth muscle; VSMC, vascular smooth muscle cell; [Ca2+]cyt, cytosolic Ca2+ concentration; siRNA, small interfering RNA; vascular smooth muscle; voltage-dependent calcium channels.