<P> Recent research indicates that sphingosine - 1 - phosphate (S1P) signaling is an important regulator of vascular smooth muscle contraction . When transmural pressure increases, sphingosine kinase 1 phosphorylates sphingosine to S1P, which binds to the S1P2 receptor in plasma membrane of cells . This leads to a transient increase in intracellular calcium, and activates Rac and Rhoa signaling pathways . Collectively, these serve to increase MLCK activity and decrease MLCP activity, promoting muscle contraction . This allows arterioles to increase resistance in response to increased blood pressure and thus maintain constant blood flow . The Rhoa and Rac portion of the signaling pathway provides a calcium - independent way to regulate resistance artery tone . </P> <P> To maintain organ dimensions against force, cells are fastened to one another by adherens junctions . As a consequence, cells are mechanically coupled to one another such that contraction of one cell invokes some degree of contraction in an adjoining cell . Gap junctions couple adjacent cells chemically and electrically, facilitating the spread of chemicals (e.g., calcium) or action potentials between smooth muscle cells . Single unit smooth muscle displays numerous gap junctions and these tissues often organize into sheets or bundles which contract in bulk . </P> <P> Smooth muscle contraction is caused by the sliding of myosin and actin filaments (a sliding filament mechanism) over each other . The energy for this to happen is provided by the hydrolysis of ATP . Myosin functions as an ATPase utilizing ATP to produce a molecular conformational change of part of the myosin and produces movement . Movement of the filaments over each other happens when the globular heads protruding from myosin filaments attach and interact with actin filaments to form crossbridges . The myosin heads tilt and drag along the actin filament a small distance (10 - 12 nm). The heads then release the actin filament and then changes angle to relocate to another site on the actin filament a further distance (10 - 12 nm) away . They can then re-bind to the actin molecule and drag it along further . This process is called crossbridge cycling and is the same for all muscles (see muscle contraction). Unlike cardiac and skeletal muscle, smooth muscle does not contain the calcium - binding protein troponin . Contraction is initiated by a calcium - regulated phosphorylation of myosin, rather than a calcium - activated troponin system . </P> <P> Crossbridge cycling causes contraction of myosin and actin complexes, in turn causing increased tension along the entire chains of tensile structures, ultimately resulting in contraction of the entire smooth muscle tissue . </P>

The involuntary movement of smooth muscles is called