Fig. 1. Proposed mechanisms of vascular smooth muscle contraction (see text for details). The location of cytosolic molecules or their translocation to the cell membrane or other subcellular sites  (e.g. , translocation of protein kinase C [PKC], Rho A, Rho kinase, or mitogen-activated protein kinases [MAPKs] to the cell membrane) is not considered in this figure. It is controversial whether Rho kinase functions upstream on, downstream on, or independently of PKC. += Stimulation; −= inhibition; AA = arachidonic acid; APL = arachidonyl phospholipids; CIF = Ca²⁺-influx factor; CaM = calmodulin; CaMKII = Ca²⁺/CaM-dependent protein kinase II; CICR = Ca²⁺-induced Ca²⁺release; Cl^Ca= Ca²⁺-activated Cl⁻channel; CPI-17 = PKC-potentiated inhibitory protein for heterotrimeric MLCP of 17 kd; DAG = 1,2-diacyl-glycerol; G = guanosine-5′-triphosphate–binding protein; IP³= inositol 1, 4, 5-triphosphate; IICR = IP³-induced Ca²⁺release; K^Ca= Ca²⁺-activated K⁺channel; LG-NSCC = ligand-gated nonselective cation channel; MLC²⁰= regulatory light chain of myosin (20 kd); MLCK = myosin light chain kinase; MLCP = myosin light chain phosphatase; PC = phosphatidylcholine; PIP²= phosphatidyl-inositol 4,5-bisphosphate; PLA²= phospholipase A²; PLC = phospholipase C; PLD = phospholipase D; RhoA-GDP = GDP-bound RhoA; RhoA-GTP = GTP-bound RhoA; ROCC = receptor-operated Ca²⁺channel; SMOCC = second messenger–operated Ca²⁺channel; SOCC = store-operated Ca²⁺channel (Ca²⁺release–activated Ca²⁺channel); SR = sarcoplasmic reticulum; TK = tyrosine kinase; VOCC = voltage-operated Ca²⁺channel.