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. Author manuscript; available in PMC: 2015 Apr 1.
Published in final edited form as: Microcirculation. 2014 Apr;21(3):219–229. doi: 10.1111/micc.12105

Figure 2.

Figure 2

Vascular smooth muscle intracellular mechanisms for vasoconstriction. Vascular smooth muscle cells (VSMC) located in the medial layer of resistance arteries reduce their length to cause vasoconstriction. This process involves mechanisms associated with the phosphorylation of myosin-light chain (MLC20), and the formation and disruption of actin cytoskeletal structures. The activation of Rho Kinase (ROCK) is an event that potentially links MLC-20 phosphorylation and actin polymerization mechanisms. ROCK inactivates myosin-light chain phosphatase (MLCP) to maintain MLC-20 phosphorylation and constriction. It also deactivates cofilin and its severing action on actin filaments via the activation of LIM kinase (LIMK). Consequently integrin linked actin fibers are able to polymerize and strengthen the cytoskeleton through processes that involve the phosphorylation of paxillin and a number of other focal adhesion proteins with and without kinase activity. GPCRs, G-protein coupled receptors; IEL, internal elastic lamina; PLC, phospholipase C; IP3, inositol triphosphate; DAG, diacyl glycerol; RhoGEF, Rho guanine exchange factor; MLCK, myosin-light chain kinase; FAK, focal adhesion kinase. Figure adapted from references 28, 47.