wave potential. These action potentials are generated by the influx of extracellular , and not . Like skeletal muscles, cytosolic ions are also required for crossbridge cycling in smooth muscle cells. The two sources for cytosolic in smooth muscle cells are the extracellular entering through calcium channels and the ions that are released from the sarcoplasmic reticulum. The elevation of cytosolic results in more binding to calmodulin, which then binds and activates myosin light-chain kinase. The calcium-calmodulin-myosin light-chain kinase complex phosphorylates myosin on the 20 kilodalton (kDa) myosin light chains on amino acid residue-serine 19, initiating contraction and activating the myosin ATPase. Unlike skeletal muscle cells, smooth muscle cells lack troponin, even though they contain the thin filament protein tropomyosin and other notable proteins – caldesmon and calponin. Thus, smooth muscle contractions are initiated by the -activated phosphorylation of myosin rather than binding to the troponin complex that regulates myosin binding sites on actin like in skeletal and cardiac muscles. Termination of crossbridge cycling (and leaving the muscle in latch-state) occurs when myosin light chain phosphatase removes the phosphate groups from the myosin heads. Phosphorylation of the 20 kDa myosin light chains correlates well with the shortening velocity of smooth muscle. During this period, there is a rapid burst of energy utilization as measured by oxygen consumption. Within a few minutes of initiation, the calcium level markedly decreases, the 20 kDa myosin light chains' phosphorylation decreases, and energy utilization decreases; however, force in tonic smooth muscle is maintained. During contraction of muscle, rapidly cycling crossbridges form between activated actin and phosphorylated myosin, generating force. It is hypothesized that the maintenance of force results from dephosphorylated "latch-bridges" that slowly cycle and maintain force. A number of kinases such as rho kinase, DAPK3, and protein kinase C are believed to participate in the sustained phase of contraction, and flux may be significant. Neuromodulation Although smooth muscle contractions are myogenic, the rate and strength of their contractions can be modulated by the autonomic nervous system. Postganglionic nerve fibers of parasympathetic nervous system release the neurotransmitter acetylcholine, which binds to muscarinic acetylcholine receptors (mAChRs) on smooth muscle cells. These receptors are metabotropic, or G-protein coupled receptors that initiate a second messenger cascade. Conversely, postganglionic nerve fibers of the sympathetic nervous system release the neurotransmitters epinephrine and norepinephrine, which bind to adrenergic receptors that are also metabotropic. The exact effects on the smooth muscle depend