Smooth muscle contraction is regulated by intracellular Ca^(2+) ([Ca^(2+)]_(i)) and the phosphorylation of myosin light chain (MLC). However, various kinds of vasoconstrictors induce a further contraction at a given [Ca^(2+)]_(i), and elicit a sustain...
Smooth muscle contraction is regulated by intracellular Ca^(2+) ([Ca^(2+)]_(i)) and the phosphorylation of myosin light chain (MLC). However, various kinds of vasoconstrictors induce a further contraction at a given [Ca^(2+)]_(i), and elicit a sustained contraction under Ca^(2+) -depleted conditions, referred to as "Ca^(2+) -sensitization", in intact and membrane-pen-neabilized smooth muscle. Previously, several molecules, including protein kinase C (PKC), RhoA, and mitogen-activated protein kinases (MAPK), have been suggested as candidate regulators of Ca^(2+) -sensitization. In the present review, we describe the role of PKC, RhoA, and MAPK in the regulation of Ca^(2+) -sensitization, and suggest a new model in research for the regulation of smooth muscle contraction.