description
The vascular smooth muscle cell (VSMC) is a highly specialized cell whose principal function is contraction. On contraction, VSMCs shorten, thereby decreasing the diameter of a blood vessel to regulate the blood flow and pressure. The principal mechanisms that regulate the contractile state of VSMCs are changes in cytosolic Ca2+ concentration ([Ca2+]c). In response to vasoconstrictor stimuli, Ca2+ is mobilized from intracellular stores and/or the extracellular space to increase [Ca2+]c in VSMCs. The increase in [Ca2+]c, in turn, activates the Ca2+-CaM-MLCK pathway and stimulates MLC20 phosphorylation, leading to myosin-actin interactions and, hence, the development of contractile force. The sensitivity of contractile myofilaments or MLC20 phosphorylation to Ca2+ can be secondarily modulated by other signaling pathways. During receptor stimulation, the contractile force is greatly enhanced by the inhibition of myosin phosphatase. Rho/Rho kinase, PKC, and arachidonic acid have been proposed to play a pivotal role in this enhancement. The signaling events that mediate relaxation include the removal of a contractile agonist (passive relaxation) and activation of cyclic nucleotide-dependent signaling pathways in the continued presence of a contractile agonist (active relaxation). Active relaxation occurs through the inhibition of both Ca2+ mobilization and myofilament Ca2+ sensitivity in VSMCs

external resources
NCBI:96530
KEGG:hsa04270
PUBMED:16870827
PUBMED:10911373
PUBMED:11679404
PUBMED:16339747
PUBMED:10221985
PUBMED:12689814
PUBMED:11165670
PUBMED:18552454
PUBMED:12060106
PUBMED:9458738
PUBMED:15725705
PUBMED:18040024
PUBMED:12693609
PUBMED:11773611
PUBMED:17158339
PUBMED:17458653
PUBMED:15026027
PUBMED:19120701
PUBMED:15269340
PUBMED:18703404
PUBMED:11709400
PUBMED:17200683

genes
ACTA2 , ACTG2 , ADCY1 , ADCY2 , ADCY3 , ADCY5 , ADCY6 , ADCY7 , ADCY8 , ADCY9 , ADORA2A , ADORA2B , ADRA1D , ADRA1B , ADRA1A , AGTR1 , ARAF , RHOA , AVPR1A , AVPR1B , BRAF , CACNA1C , CACNA1D , CACNA1F , CACNA1S , CALD1 , CALM1 , CALM2 , CALM3 , CALML3 , CYP4A11 , EDNRA , GNA11 , GNA12 , GNAQ , GNAS , GUCY1A2 , GUCY1A1 , GUCY1B1 , ITPR1 , ITPR2 , ITPR3 , KCNMA1 , KCNMB1 , MYH11 , MYL6 , MYLK , PPP1R12A , PPP1R12B , NPR1 , NPR2 , PLA2G1B , PLA2G2A , PLA2G4A , PLA2G5 , PLCB2 , PLCB3 , PLCB4 , PPP1CA , PPP1CB , PPP1CC , PRKACA , PRKACB , PRKACG , PRKCA , PRKCB , PRKCD , PRKCE , PRKCG , PRKCH , PRKCQ , PRKG1 , MAPK1 , MAPK3 , MAP2K1 , MAP2K2 , PTGIR , RAF1 , ROCK1 , PLA2G6 , PLA2G10 , PLA2G4C , JMJD7-PLA2G4B , ARHGEF1 , ROCK2 , ARHGEF11 , CALCRL , KCNMB2 , RAMP2 , RAMP1 , RAMP3 , MRVI1 , MYL9 , GNA13 , PLCB1 , ARHGEF12 , PLA2G2D , KCNMB3 , KCNMB4 , PLA2G2E , PLA2G3 , CALML5 , PPP1R12C , PLA2G2F , PLA2G12A , PLA2G12B , MYLK2 , MYLK3 , CALML4 , PPP1R14A , PLA2G4E , MYL6B , KCNU1 , CALML6 , ADCY4 , PLA2G4F , PLA2G4D , CYP4A22 , MYLK4 , PLA2G2C , PLA2G4B ,